Episode 9 Season 7: Shingles, Dog Context, and The Immune System with Dr. Mohseni

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On this week's show we dive into the hidden connections between shingles vaccines and decreased dementia risk, while exploring how humans often misinterpret their pets' emotions based on environmental context rather than actual animal behavior.  Our guest, Dr. Yasmin Mohseni blows us away with the inner workings of the immune system.

Some highlights:

• Shingles vaccine study reveals a 20% reduction in dementia risk, particularly among women
• The protective effect may be linked to how viral infections modify the immune system
• Humans heavily rely on situational context rather than dogs' body language when assessing canine emotions
• A study of 400 college students showed they couldn't distinguish dog emotions without environmental cues
• Dr. Yasmin Mohseni explains why the immune system isn't a simple on/off switch that can be easily "boosted"
• Immunotherapy approaches like CAR T-cell therapy are revolutionizing cancer treatment
• Cancer cells create "fortress-like" defenses that engineered immune cells must overcome
• Understanding your pet's actual body language rather than situational context can improve communication

Dr. Yasmin's links:

Instagram: https://www.instagram.com/doctor.yas_/

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Episode Transcript

Speaker 1 (00:09):
Hello science enthusiasts.
I'm Jason Zukoski.
And I'm Chris Zukoski, we'rethe pet parents of Bunsen,
beaker, bernoulli and Ginger.

Speaker 2 (00:18):
The science animals on social media.

Speaker 1 (00:21):
If you love science.

Speaker 2 (00:22):
And you love pets.

Speaker 1 (00:24):
You've come to the right spot, so put on your
safety glasses and hold on toyour tail.
This is the Science Podcast.
Hello everybody and welcomeback to the Science Podcast.
We hope you're happy andhealthy out there.
This is episode nine of seasonseven.
It's a little late coming outtoday.
Chris and I did our best to getit out on Saturday.

(00:46):
Normally the podcast comes outon Friday.
We had a really exciting andbusy week and we ran out of gas.
The Bernoulli stuffy launchedto the public this week and we
had an amazing response.
So thank you so much toeverybody who supported us by
picking up a Bernoulli stuffy inour pre-sale campaign.
And then Friday Bernoulli gotto play with Chesney, his

(01:10):
favoritest dog.
Chesney is a service and thedog of the amazing Marla Smith,
who does great work fordisability advocacy on social
media.
So we're a little late, butwe're here to do it now.
All right.
In science news we're going tobe looking at a protective
effect the shingles vaccine mayhave on folks who got it.

(01:31):
And in pet science, are youreading your pet emotions wrong?
Chances are.
It depends on the context.
Our guest and ask an expert isDr Yasmin Mousseni, also known
as Dr Yas.
Ask an expert is Dr YasminMousseni, also known as Dr Yas,
on social media.
She's going to be talking to usabout the immune system in an
amazing interview.
Okay, let's get on with theshow, because there's no time

(01:52):
like science time.
This week in science news,let's talk about disease caused
by a virus I think both you andI got when we were young, chris.

Speaker 2 (02:06):
The chickenpox virus.

Speaker 1 (02:08):
Yeah, specifically the viral infection that you may
get when you're older calledshingles if you were infected
with chickenpox.
Do you remember gettingchickenpox?
I don't, but there are photosof me and my brother Cam covered
in chickenpox bumps.

Speaker 2 (02:25):
Mm-hmm.
Yeah, both my sister and I gotchicken pox when we were younger
and actually she got some kindof significant scarring because
she was very itchy and veryscratchy like the cartoon.
Itchy and scratchy, but I don'tthink my case was as extreme as
hers, but we both definitelygot the chickenpox.

(02:48):
Duncan was born in 1997.
So I do remember when he wasgoing for his vaccinations, his
routine vaccinations they didask hey, did your child get
chickenpox?
And I said yes, I believe hedid.
And they said we have thisvaccine, would you be interested
in getting the vaccine as well?
But then they said we don'tnecessarily need to vaccinate if

(03:10):
he's already had the virus.

Speaker 1 (03:12):
Oh, did Duncan get chickenpox?
I forget.

Speaker 2 (03:14):
Yeah, he did as a child.

Speaker 1 (03:17):
Man, that was so long ago.
It must not have been very bad.

Speaker 2 (03:21):
No.
And then it makes you questionlike like did my child get
chicken pox?
I?

Speaker 1 (03:24):
totally forgot and you just want to be sure to give
them the best chance and keepthem the most healthy now we're
not going to be talking aboutchicken pox, we're going to be
talking about shingles, andafter you recover from chicken
pox the virus lies dormant inyour nerve tissue and then can
reactivate later in life asshingles.

(03:46):
So maybe that's something youand I can look forward to as we
get a little older.
But your dad and stepdad bothsuffer from shingles flare ups
from time to time, and I thinkLissa too, your niece.

Speaker 2 (04:00):
Yeah, but you don't have to wait till you're old.
Melissa is 31 and already hashad shingles very bad.

Speaker 1 (04:09):
So it's a really painful rash and a band on one
side of the body that you can becovered with it, like it's not
like chicken pox, it's a rash,and people who have it they
report that it feels likethey're on fire, like it's
burning, tingling or it's numbbefore the rash appears, and
then the rash itself is reallypainful and it actually can

(04:32):
cause significant nerve pain,vision or hearing loss and then,
in really bad cases of shingles, flare-ups, neurological
complications.
So it's not fun, it's no joke,that's for sure.
And then, in really bad casesof shingles flare-ups,
neurological complications.
So it's not fun.

Speaker 2 (04:46):
It's no joke, that's for sure, and what we're
covering today is a studypublished on April 2nd in the
Nature magazine, and that studyinvestigated if receiving a
vaccine with a live virus it'scalled the live attenuated
shingles vaccine and if thatlowers the risk of developing

(05:08):
dementia.
And they use data from a Welshvaccination program starting in
2013.

Speaker 1 (05:17):
And that live attenuated version is.
It's a weakened version.
It's not the live virus.
It's a weakened version.
It's not the live virus.
So it gives you an immuneresponse.
I guess it gives them the ideathat you're infected with
chickenpox or shingles, but youdon't actually get it.
I think in very rare cases thevaccine can cause.

(05:39):
In a live attenuated vaccine itcan cause it, but those are
extremely rare circumstances.
So this study focused on olderfolks who were born between
September 1st 1925 and September1st 1942.
And they used a naturalexperiment design.
It compared people born justbefore and just after the

(06:02):
vaccine cut off, which was 1933.
I believe that at that pointthey'll suggest you don't get
the vaccine.
So that's why there's thateligibility cut off.
This approach minimized biasfrom health conscious behavior,
so people who chose vaccines mayalso choose other healthy

(06:23):
habits.

Speaker 2 (06:24):
That's right.

Speaker 1 (06:25):
That can influence your risk of dementia.

Speaker 2 (06:27):
Comparing individuals born just before and after that
date did create a naturalexperiment similar to a
randomized control.
It identified a situation wherepeople who get the treatment
the shingles vaccine and theywere not really different from
people that were much lesslikely to get the vaccine, and

(06:48):
so it eliminated that bias.

Speaker 1 (06:51):
Because you want as little bias as possible in
science studies.
After they got all the datafrom the folks before and after
this cutoff, diagnoses fordementia dropped at the vaccine
eligibility threshold.
So those who got the vaccinehad a 20% relative reduction and
it's not a crazy reduction.

(07:12):
It's not like you will not getdementia if you got the shingles
vaccine.
It was just an interestingconclusion from looking at all
the folks who were at risk forit and got to the vaccine.

Speaker 2 (07:24):
One thing that is more interesting is the
protective effect was moreprominent in women.
They did not see a statisticalsignificant difference observed
in the men, and this may be dueto gender-based immune system
differences in relation to howyour body reacts to the vaccine

(07:44):
and the immuno response that youget.

Speaker 1 (07:46):
The study had some ideas, as I mentioned, why that
may be.
Shingle infections are linkedto dimension development and it
might modify your immune systemin ways not understood that
delay or prevent dementia and,as you said, chris, much more
prominent in women.
Another kind of like thing weshould also say is that the
study focused on the earlyvaccines that folks got the live

(08:09):
attenuated shingles vaccine.
That was one dose using theweakened virus.
This vaccine was discontinuedin 2020, and it was replaced by
another vaccine called therecombinant shingles vaccine.
You get two doses and there'sno live virus, and a later study
from 2024 suggested that thisvaccine may be even more

(08:32):
effective in reducing dementiarisk.
So the authors of this studyare going to be looking, perhaps
, at those folks, but they justneed a little bit more time
because that's a really newvaccine and I guess they just
got to wait for folks to get oldenough that they're more at
risk to developing dementia.

Speaker 2 (08:49):
But I don't think that throwing out the evidence
from the live attenuatedshingles vaccine is something
that would be beneficial,because it does show that
decline in dementia and it'ssomething that can be studied
more.

Speaker 1 (09:03):
Yeah, for a disease that isn't 100% understood, I
think the more we know about itthe better.
That's science news for thisweek.
This week in pet science we'regoing to be looking at a study
on dog emotions.
Do you think you can tell whenBunsen, beaker and Bernoulli are
happy, chris?

Speaker 2 (09:23):
I can tell when they're happy, but this study
puts that kind of how can youtell your dog is happy?
Into it.
Does it with a twist?
So for me, because I'minteracting with the dogs and I
see what's happening around intheir environment, I can see, oh
, the Amazon or the deliverypersons here and Bunsen's at the
door and he's on alert and he'sbarking.

(09:44):
I might attribute that to thefact that, alert, there is a
delivery person coming andBunsen is protective of the
house, whereas if I saw that, ifhe was outside and just barking
, maybe I would think it wouldbe a different reaction to
something.
Yeah, it's the contextdifferent reaction to something.

Speaker 1 (10:04):
Yeah, it's the context that we are heavily
influenced by.
That's what the study isgetting at, though I think when
Chesney and Bernoulli wereplaying, I think they were both
pretty happy.

Speaker 2 (10:16):
Oh, they were so happy, jason, they loved each
other.
But they are able to pick up ontheir social cues and chesney
did a really great job ofputting bernoulli into line.
No, I don't want that behavior.
And he respected her and hepicked up on her cues and he

(10:37):
changed or modified his behavioraccordingly.
I think, as humans though, likeyou, definitely don't like the
being amorous, and that's fair.
And as humans, did we read thebehavior and then jump into
quickly before Chesney had achance to change it, so being

(10:57):
able to read the behavior, butthen also, having said that, you
don't want the behavior to gotoo far.
So if the dog is in a littlebit, giving warning, are we
reading the body languageappropriately, and if we don't
step in soon enough, then itcould lead to something far more
nefarious or dangerous.

(11:20):
So, it's hard to tell.
It's hard to tell.

Speaker 1 (11:22):
It is, and I think that's where we can get to the
study crest, because HollyMolinaro, an animal welfare
scientist at Arizona StateUniversity, thought to test
those contexts.
She used her dad's dog, oliver,who's an older 14-year-old
pointer beagle mix, and Oliverwas filmed in a variety of

(11:43):
positive and negative scenarios,like being praised, played with
, and negative, like beingscolded, and in the study it
says around a cat.
So that would Bernoulli wouldfit in right there around Ginger
.
There were 400 college studentsthat were shown edited footage
of Oliver on a black backgroundstripped of all of the

(12:05):
environmental context.
Ah, so just Oliver and uneditedfootage.
After viewing, the participantswere asked to assess Oliver's
emotional state, which is cool,because can you look at the dog
and determine if it's happy orsad without the context of being

(12:27):
scolded or being played with?

Speaker 2 (12:30):
I know, and what they found was in the edited footage
participants couldn'tdistinguish whether Oliver was
happy or sad.
Only after viewing the uneditedfootage allowed them, the
participants, to accuratelyidentify Oliver's emotions.
So this suggests that peopleheavily rely on context rather

(12:55):
than dog behavior alone toassess the emotions of the dog.

Speaker 1 (13:00):
And here comes the twist.
A second group of 513participants were shown edited
clips where positive behaviorwas shown in a negative context
and negative behavior was shownin a positive context, in a
negative context.
A negative behavior was shownin a positive context.
So example Oliver was reactingto a vacuum cleaner, but it was

(13:21):
edited to appear like he wasreacting to a toy.
And what did they find there,chris?

Speaker 2 (13:27):
What they found was that, no matter what Oliver was
actually doing, people basedtheir interpretation solely on
the surrounding context.
So if the context lookedpositive, they assumed Oliver
was happy.
Conversely, if the contextlooked negative, they assumed
the dog was sad.

Speaker 1 (13:49):
So some of the key takeaways that I think we should
think about as dog parents isyou probably should be careful
generalizing results from asingle dog.
This is just Oliver, and dogslike Oliver with floppy ears are
harder to read compared to dogswith more pointy ears.
And Bernoulli and Bunsen havethe little eyebrows that move

(14:12):
around when they're emoting,which gives their face like a
very cartoony like expressionwhen they're happy or scared or
sad, whereas Beaker's face canbe very muted, like when she's
happy, but if she's not happyyou don't know what she's
thinking because she's justlooking.

Speaker 2 (14:29):
So when she's just existing, her face doesn't
necessarily emote.
Existing, her face doesn'tnecessarily emote.
And we love it when she's happybecause then, like when she's
going for a walk, you can tellthere's an instant change in her
demeanor yeah, we call herblank expression that she has

(14:52):
her rbf, which is resting beakerface yeah, that she has her RBF
, which is resting beaker face,yeah, which we think is funny.
The study emphasizes that humansoften misread dog emotions by
focusing too much on theexternal cues rather than the
body language, and dog ownersare advised to practice focusing
more on the dog's physical cuesthan the environmental factors,

(15:14):
and I think that's what we'vedone a lot watching our dogs in
terms of their behavior,especially with Beaker as a
COVID puppy.
She slinks a bit and she exudesthat overconfidence with other
dogs but really she's not aconfident dog and it's oxymoron
or a paradox in her behaviorbecause you think oh, wow,

(15:34):
she's's barking, she's liketrying to make herself look big
because she's obviously veryconfident, but it's actually the
opposite she's puffing up to beI'm big, because I actually
feel not confident and one thingthat we're doing to mitigate
that is definitely taking her towaggles and she's able to play

(15:55):
with other dogs and gain thatconfidence which has been so
amazing for her.
She's been making friends.

Speaker 1 (16:02):
The strongest contexts are, as you said, the
dog's body language, like theirtail position, their ear
position and their facialexpressions.
So you have to remove thecontext and look at what the dog
is doing, not what theenvironment is doing to the dog,
and that's easier said thandone.
All right, that's Pet Sciencefor this week.

(16:23):
Hello everybody, here's someways you can keep the Science
Podcast free.
Number one in our show notessign up to be a member of our
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It's an amazing community offolks who love pets and folks
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We have tons of bonus Bunsenand Beaker content there and we

(16:44):
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It's tons of fun.
Also, think about checking outour merch store.
We've got the Bunsen Stuffy,the Beaker stuffy and now the
Ginger stuffy.
That's right, ginger thescience cat has a little replica
.
It's adorable.
It's so soft, with the giantfluffy tail, safety glasses and
a lab coat.

(17:04):
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family and friends to listen too.
Okay, on with the show Back tothe interview.
It's time for Ask an Expert onthe Science Podcast and I'm
thrilled to have expert inimmune therapy, dr Yasmin

(17:25):
Mohseni, with us today.
Doc, how are you doing?

Speaker 3 (17:28):
I'm good, thank you.
Thank you for having me on.
How are you doing?

Speaker 1 (17:31):
I'm good.
My wife and I are big fans ofyour Instagram page, so we're
really excited to have you on.
You do a great job withteaching us all about the immune
system and it's just a thrillto have you on our show.

Speaker 3 (17:42):
Thank you so much.
Thank you, I'm a massive fan ofyour page as well.
Your page always makes me smile, and just the dramas between
Benulli and Ginger.

Speaker 1 (17:52):
Oh man, it's drama llama at our house.
I tell you that.
Where are you in the world,where are you calling into the
show from?

Speaker 3 (18:00):
I'm actually in Los Angeles at the moment.
Yeah, I moved here three yearsago.
It's been just over three yearsnow, but I was in London for
all of my life, so I trainedthere as well.
I was briefly outside of Londonfor my undergraduate degree,
but, yeah, then the opportunityarose to move to the States and
I got to the age where it waslike, oh, it really is now or

(18:20):
never.
So I thought, trade the rainand depressing weather for the
sun and the life in LA.
Why not?
Let's give it a go, and I'm sohappy I made that decision.

Speaker 1 (18:30):
Nice and were you safe from the fires?
That's been all of our Canadiannews.
Were you safe?

Speaker 3 (18:34):
from the fires.
That's been all of our Canadiannews.
Yes, it was a bit hectic,because for a while we were okay
.
But then there was this newfire, called the Kenneth Fire,
that popped up somewhere out ofnowhere and we basically had a
two-hour window to just get out,which was very jarring.
And so we both went home fromwork, we packed up the cats,

(18:57):
packed up suitcases quick, quickand we just went and stayed
with a friend, but luckily thatfire got contained really
quickly.
But yeah, that was definitelyan experience.
Of course, no power as well.
So it's yeah, january was alittle bit nuts in LA, but
luckily things seem to besomewhat coming back to normal,
I think that's good, I'm glad.

Speaker 1 (19:14):
I'm glad you're okay and like your property and
obviously your animals are okaytoo.
Yeah, so I introduced you as adoctor and you're known as Dr
Yas on Instagram.
Can you chat with us just alittle bit about your education
background in science?

Speaker 3 (19:28):
Yes, of course.
So I've trained as animmunologist.
I got my PhD from King'sCollege London, so initially I
trained.
My bachelor's degree was inbiochemistry.
So if we're going to go all theway back in time, I was
studying at Warwick Universityand it was quite funny because
when I came to the end of mydegree I panicked, thinking as

(19:51):
we all do what am I supposed todo with my life, my career?
And I thought let me just do amaster's degree just to buy
myself some time to figure outwhat I'm meant to do.
And my master's degree, Idecided, would be in immunology,
where I studied at ImperialCollege London, which is a
really fantastic institution,london and I ended up

(20:12):
specializing in allergies, whichI found was so fascinating.
But I realized I just had morequestions after my master's
degree and I thought I can'tenter the job space now.
I need to understand a bit moreabout the immune system.
Because I was so captivatedduring my bachelor's degree
where it just seemed like allthese cells function in almost

(20:32):
somewhat of a society and theyall have these different
designated roles just tobasically keep us alive every
day.
And it was the humanizingelement of the immune cells this
guy has this job goes andactivates this guy.
This guy then goes and followsthe call and goes to this area.
I just thought this is insane.
This is crazy, how this is allcells and I think I don't know.

(20:57):
There was this video, whichactually I think I'll upload it
on my page because it's sofascinating.
That really got me captivated.
It was just this picture of animmune cell chasing after a
piece of bacteria and I thoughthow is this happening?
I have to understand more.
So that led me to my master'sand then, as I said, I had more
questions and I wanted to thengo on to do a PhD and I ended up

(21:21):
getting the position at King'sCollege London where I was
specializing in organ transplantrejection and autoimmunity.
It was like developing a type oftherapy to hopefully try and
stop liver transplant rejection.
But that type of therapy tohopefully try and stop liver
transplant rejection, but thattype of therapy could also be
applied to autoimmunity, becauseessentially it's kind of some

(21:42):
I'm gonna say this like it'svery nuanced but similar
mechanisms in the sense oftrying to regulate the immune
system, because when you have anorgan transplant, your immune
system is rightfully doing thecorrect thing by trying to
reject it because it'srecognizing it as foreign.
It's not you.
So you have to be put onimmunosuppressants to try and

(22:03):
stop that transplant from beingrejected, and similarly with
autoimmunity that is more yourimmune system going wrong,
though, and your immune systemturns on you and starts
attacking you.
So if you can employ similarmechanisms of just trying to
regulate the immune systemsomehow.
So that was what my phd was,and it was very hardcore, very

(22:25):
savage, but also very enjoyable.
I learned a ton, and Ispecialized in a type of cell
called a t-reg, and the t-regsin the immune system are the
main cells that quiet the immunesystem.
They switch it off.
Essentially, they controlinflammation.
So by knowing you have thesecells that control inflammation,
that stop the immune, basicallystop inflammation from

(22:49):
happening, quiet the immunesystem, you can use them
essentially in a therapeuticcontext to hopefully stop organ
transplant rejection orautoimmunity.
So that was my PhD, and then Iwent on to a startup, which was
founded by my professor and fiveothers, basically using that

(23:10):
technology in a liver transplantsetting, and I know they've
gone on to be quite successful.
I think they've got likemultiple autoimmune programs now
.
I think they've just signed alot of money with AstraZeneca or
something to be able to fundthe pipeline project, for I
think it was IBD or neuro, butpretty amazing stuff.

(23:31):
But then I segued over to theUS and I came over here three
years ago and now I've actuallyjumped into the cancer space, so
still using a type ofimmunotherapy to hopefully cure
solid tumors.
So that's my career and whereI'm at so far.

Speaker 1 (23:51):
I appreciate the roundup there.
Yeah, I felt like a little bitof a.
I felt like I was a bitignorant because I just learned
last week as a grown man thatpeople with organ transplants
they have to take thoseimmunosuppressants for probably
their whole life.
I didn't know that.

Speaker 3 (24:11):
Yeah, it's one of those strange things, but
probably the reasons why youdidn't know that is because
there's such a focus on findingmatched transplant donor, like
matching on the blood type, andwhile we've done a fantastic job
in that regard to stop acuterejection from happening, sort

(24:34):
of, the antibodies kick off fromthe get go and then round up
the rest of the immune systemand just obliterate the organ,
the organ transplant, we stillhave this risk of chronic
rejection essentially happeningwhere you can match as close as
possible, but ultimately youwill have these minor antigens,
we say, or like minor, minor,minor, we could say proteins
that really are your blueprint,that distinguish you from

(24:58):
someone else.
And no matter how closely youtry and match, your immune
system is so highly specializedand evolved to be able to
distinguish.
I think one of the hallmarks ofthe immune system is its
ability to distinguish you fromnot you.
So that is why, even if youfollow all the protocols to
match patients accordingly todonors, yes, you will stop that

(25:22):
acute rejection from happening,but it's very hard to stop that
chronic rejection from happeningbecause ultimately your immune
system can tell you from, notyou.
So, yes, you go onimmunosuppressants and the
problem tell you from, not you.
So, yes, you go onimmunosuppressants and the
problem, excuse me, withimmunosuppressants is that they

(25:43):
don't fully halt the immunesystem.
Immunosuppressants have, like,different mechanisms.
They might target these cellsor these pathways or general
bring down, like the sort offunction and development of B
cells and T cells, which areyour adaptive arm of the immune
system, but they don'tcompletely wipe them, and for
good reason.
You need your immune system,don't you, to survive.
So that means that your immunecells still have this image of

(26:08):
coming round here and there andtaking jabs where they can at
the transplant.

Speaker 1 (26:12):
So it's the drive-by just punches it in the face
every now and again Exactly, itwas like, oh, that's my chance
punch.

Speaker 3 (26:22):
But then that reality is that the half-life of organ
transplants.
I think it differs, but we knowballpark.
We say about maybe 10 to 20years for liver transplants.
I do not know if that's changedsince I've left the field five
years ago.
Liver transplants I do not knowif that's changed since I've
left the field five years ago,but you will probably, if you
are a young recipient, you'llprobably need another one in
your lifetime, unless if weanother transplant in your

(26:43):
lifetime, unless if we reallyoptimize the therapies.
So that's the big issue.
And the other issue isimmunosuppressants, especially
to this scale for organtransplantation.
They're really hardcore on thebody right.
They usually take a massive jabat your kidneys as well, so
they're like nephrotoxic, andalso just the fact that, yeah,
you're suppressing your immunesystem, which isn't great, given

(27:04):
we're living in a world whereeverything is trying to kill us.
So we need other options,essentially, and that's where my
career as an immunologist began.

Speaker 1 (27:14):
Yeah, there's folks like you working on it, which is
amazing.

Speaker 3 (27:17):
Trying, trying my best.
As I say, I've moved out of itnow and I've gone into the
cancer field, but my passionreally is back in regulation.
So I do think at some point Iwill move back into the space of
autoimmunity and organtransplant rejection.
But we'll see.
We'll see how it goes.

Speaker 1 (27:34):
Yeah, it's all good.
You know that was mymisconception.
Are there other misconceptionsabout our immune system that you
hear or you just like to telleverybody?
I'd love to know like, fromyour perspective, one of the
misconceptions that you seeabout the immune system in
general.

Speaker 3 (27:54):
Yeah, so I think this was.
This is an interesting questionbecause I think this was one of
the reasons why I decided tostart my science communication
page on social media Just peopleneeding to realize that the
immune system is not a binary onoff switch.
I think that's the biggesttakeaway I want people to try to

(28:17):
understand.
There is this literature, inthe literature nomenclature
words such as immune boostingand immune resetting, and that
is not completely accurate,unless if we want to talk about
in the conventional therapycontext where, yes, we do have

(28:37):
these mechanisms in place, orlike rather hardcore protocols
to be able to quote-unquotereset the immune system.
But we're talking about reallyhardcore, like full
myeloablation, like intensechemotherapy and then rebuilding
with bone marrowtransplantation, for example, in
like for cancer, patientsettings or blood disorders.

(28:58):
There's other interesting thingsin my field where we're using
the concept of immune resettingby targeting patients with
autoimmune diseases.
So we're using a therapy toessentially ablate completely
these naughty T cells and Bcells that are causing
autoimmunity and then, ifthey're gone, and then obviously

(29:20):
over time you rebuild yourblood, stem cells kick in and
then you rebuild a new immunesystem.
I say new, not just like youjust have new cells developing,
then yes, in theory you havereset the immune system.
But in this long roundabout wayI'm trying to say I'm seeing
alarming protocols online fromthe wellness community on with

(29:43):
bold claims that, following ABCtaking this pill, doing this
protocol, doing this sort ofcold plunge or even like just
walking into Erewhon, do youguys have arrow one?
It's this very fancysupermarket or grocery store
that's very upmarket from wholefoods.
It's very la.
You always see celebrities inthat but arrow one it's called

(30:07):
arrow one is e.
I'm probably butchering thatword in my accent, but e r,
e-o-n is like this super fancysupermarket and I walked in.
I was like this is ridiculous.
How expensive everything ishere.
It's very elegant, but anyways,point is like this when you go
walk through era one, everythingis like immune boosting.

(30:27):
This drink, that's what'simmunity boosting and I just
thought this is, I like justchuckle to myself, because it's
really not that easy to be ableto reset or boost your immune
system through a simple pill.
I just think the biggestmisconception here is, I think,
people, I would like people toalmost not disrespect the immune

(30:48):
system that's been evolving formillions of years.
Essentially and I don't meanthat disrespect to any
influencers that are claimingit's all out of good faith and
trying to help people that aredesperate with their health but
says with the utmost sinceritybut even immunologists, we're
still grasping the complexitiesof the immune system.

(31:09):
Any sort of central dogma thatwe believed about the immune
system is constantly gettingflipped on its head.
Now I'm always getting baffledby new findings that we're
understanding about the immunesystem, about just basically,
from immune cells shape-shiftinginto different roles that we
didn't classically define them,from having in the body, maybe
because of adaptation, in a goodway or in a bad way in certain

(31:32):
situations.
I think a perfect example I cangive is my story.
At least during my PhD, Ideveloped I say I developed I
attempted to develop thisprototype proof of concept, as I
said, to try and cure organtransplant rejection.
So what I did was I developedthis type of therapy called a

(31:53):
CAR-T reg therapy, which we cantalk about in detail later or
another time.
But what I did, teamed up withmy professors, of course, to try
and make it super effective, isby making it produce a crap
load of anti-inflammatoryproteins.
Because the idea was, once youinject it into the patient and

(32:14):
if you have this therapy that'ssuper anti-inflammatory and
target it to this organtransplant, then you're going to
create this sort of environmentthat's very anti-inflammatory.
Therefore, hopefully, youshould logically stop organ
transplant rejection, because ifthere's an anti-inflammatory
effect, then any T cells or Bcells that come along and try

(32:34):
and take jabs at it arebasically dampened.
What I found when I createdthis therapy and put it in my
mice was it was extremely toxicfor the mice and actually caused
the opposite effect.

Speaker 1 (32:47):
Whoa.

Speaker 3 (32:49):
Super inflammation, whoa.
And then time was up and I hadto write my thesis and I was
like I couldn't even expand onit further, so it was very
disheartening.
So that's the thing.
It's the fact that we Iexpected it to have this one
effect cause the completeopposite effect, this intense
pro-inflammatory response.

(33:10):
To any immunologists out there,it was aisle 10, so if they
want to go and look that up,they know what IL-10 is, but
it's basically a.
It's something called acytokine, but we can just, for
lay terms, call it a proteinthat is just known to be super
anti-inflammatory, yet suddenlyproducing so much of it was
causing this opposite effect ofmass inflammation.

(33:31):
So that's what I'm trying to sayis that the immune system is so
complex it doesn't follow therules that we expect it to, and
not even on the individual celllevel and their individual jobs,
but even combined with othersystems.
I mean, we're now looking atneuro endo immuno axis, for
example, like the interfacebetween neuroscience,

(33:53):
endocrinology, for example, likethe interface between
neuroscience, endocrinology, theimmune system, I don't know
psycho endo immuno.
It's just like we have to lookat this holistically, and when I
say holistically, it's our bodyas a whole.
Our immune system isn'tsomething that's separate from
our neuroscience, endocrinologyand all the other systems and

(34:14):
cells will adapt accordinglyneuroscience, endocrinology and
all the other systems and cellswill adapt accordingly.
So that was the biggestmisconception, that now I'm
switching at least the goal ofmy page to try to educate people
a little bit more on this.
It's not so easy to reset oreven boost your immune system by
at least non-conventional,non-invasive treatments.

(34:34):
I hope that makes sense.

Speaker 1 (34:36):
It's a little more complicated than eating
probiotic yogurt and taking awalk in the sunshine.

Speaker 3 (34:42):
Exactly, but all those things help.

Speaker 1 (34:43):
They help true.

Speaker 3 (34:46):
That's the thing.
I'm not necessarily an expertin this area, yet I'm trying to
grow in knowledge myself interms of all the basics.
But people do neglect thebasics, like to support I'm not
going to say boost or reset, butto support your immune system,
like exercise, stress management, nutrition, staying up to date

(35:06):
with vaccinations Like these arethe pillars of a
well-functioning immune system,and by getting these basics
right, you don't need tonecessarily be faffing with
these other protocols to thatyou saw online by some
influencer to optimize yourhealth.
Now, forgetting that lastsentence, I mean by getting
these basics right, unless ifyou are someone that is dealing

(35:28):
with immune related diseases,then of course, additional
interventions may be necessary.
Then of course, additionalinterventions may be necessary.
But, yeah, start with thebasics and just know that it's
not that easy to reset or boostyour immune system, but we just
need to move to using newlanguage such as supporting your
immune system.
I would say yeah, that's.

Speaker 1 (35:49):
I so agree.
The pillars are important andyou need to support them.
But just having one crazystrong pillar does not a house
make.

Speaker 3 (35:58):
No, no, and that is funny.

Speaker 1 (36:00):
you mentioned the cold plunging things.
Those got really popular uphere in Canada in the winter
because it's cold all the time,so you could just go outside and
hop into some water and youhave your cold plunge ready for
you.

Speaker 3 (36:12):
I mean I'm not, as I say like I mean I need to maybe
fact check myself here in thisarea.
I'm still growing and trying tounderstand more about all these
other ways to optimize my ownimmune system, because I'm also
myself dealing with immunerelated issues.
It always seems ironic thatwhatever you end up specializing
in you yourself end up actuallypotentially getting riddled

(36:33):
with the issue itself.
Yeah, which we always I'm openabout this on social media about
about it as well.
But with cold plunges, I'm surethere are other, like a bunch
of other benefits that peopleare exploring at the moment.
That's why it's gained a lot ofpopularity.
But in terms of the shockfactor, I mean there are other

(36:54):
ways to definitely shock yourimmune system as well, like as
well as a cold plunge.
So, yeah, it's just fascinatingto see the obsession these days
with all these potential waysto boost your immunity.
So I'm learning myself of whatpeople are interested in trying
out.

Speaker 1 (37:10):
There you go, Though.
For anybody listening, all youhave to do is go for a swim off
the West coast of VancouverIsland.
That's your cold plunge.
So, you can get your wetsuit onand get some surfing.

Speaker 3 (37:22):
There you go Cold plunge also are you supposed to
get your wetsuit on?
I don't know.
Are you supposed to just justgo for it?
Isn't that a proper cold plunge?

Speaker 1 (37:30):
or are you at risk of serious hypothermia, which I
know, just because we vacationedout there and the ocean is
chilly, very cold.
So it's way more comfortable togo surf, for example, with uh,
with your wetsuit on than justin a bathing suit.
I'm not sure how long you'dlast, yeah.

Speaker 3 (37:49):
I don't think so.
I don't know either.
Highly recommend theCalifornian sun, of course.

Speaker 1 (37:55):
Hey, can I ask you a question about what you're
looking at now with your switchto cancer?
Is that something we can talkabout just real quick?

Speaker 3 (38:04):
Absolutely, I could talk about this for ages.
Yes, okay, so a little bit aboutthe technology.
So immunotherapy has it'sbasically revolutionized
healthcare One type ofimmunotherapy called immune
checkpoint inhibitors thatactually won the Nobel prize in
2018.
And it's now considered apillar or a staple for treating

(38:25):
cancer essentially.
So it's sort of the clue is inthe name of immunotherapy.
It's finding ways to enhanceyour immune system to treat
various diseases, and that'seither helping your immune cells
that are already there andgiving them something to quote,
unquote, turbo, turbocharge themagainst cancer, or that there

(38:46):
is a type of therapy called CAR,t-cell therapy, which so CAR,
like C-A-R and T-cell therapy,which I'm in that space, and I
was in that space for organtransplantation as well, but an
autoimmunity but yes, I've movedin for cancer now where
essentially, what you do is youtake a cancer patient's T-cells
out and you engineer them with,basically, the ability to hunt

(39:11):
down the specific cancer thatthey have.
And you grow them to like themillions and millions.
Ideally you try and achievebillions of these T-cells that
are engineered outside the body,so in a manufacturing facility,
and then you re-infuse thepatient now with these depending
on the dose level hundreds ofmillions of T cells that are now

(39:33):
armed with this ability, like aGPS, to go hunt down that
cancer.
So that is what I'm doing atthe moment.
It is really cool, it's reallybadass.
It's been changing the game,especially for blood cancers
like leukemias.
We know that a lot of patientshave been effectively I'm

(39:55):
hesitant to say the word cured,but effectively cured or at
least in long-term remissionbecause of CAR T cell therapy.
So we're realizing weaponizingyour immune system really is the
future of sort of health andlike health interventions.
So that's what I'm doing at themoment.
I absolutely love it.

(40:15):
And cancer is a reallycomplicated one because it fight
the cancer cells.
It's scary because they fightback and your immune system part
of what your immune system'sjob is basically to go and look
for cancer.
So right now in your bodythat's what your immune cells
are doing.
Your immune cells are going andbasically taking like a
register, like the classregister, just to check that all

(40:36):
the cells.
I know, that's the image that Ihave.

Speaker 1 (40:39):
It's like I love it.
That's a great analogy.
I'm sorry, continue, I justchuckled because I'm a classroom
teacher.

Speaker 3 (40:45):
Oh, of course.
Yeah, so you're effectively anNK cell, a natural killer cell
that's walking, floating around,buzzing around, taking the
register to make sure thateveryone is in check, everyone's
behaving well, and then whathappens is when they encounter a
cell that's stressed out,because stressed out cells, like
cancer cells, they become thesort of neat we call it

(41:06):
neoplastic like they change.
So when they change and becomecancerous, they basically can
also emit, like these dangersignals or do these other things
where they pull in receptorsand perhaps not knowingly,
because cancer cells, especiallywhen they become more advanced,

(41:27):
they try and evade the immunesystem because they know that
the I say they know as if, like,we're putting some sort of
humanizing thinking element toit, but they quote unquote know
that the immune system is tryingto hunt them down and kill them
essentially.
So the immune system then kicksinto gear once they've detected

(41:49):
that we do have a rogue cancercell that's arisen.
But unfortunately this battlethat's ongoing causes your
immune cells to become exhausted.
So that's the term immuneexhaustion or t-cell exhaustion
kicks in like they get.
They're basically justconstantly fighting and they
become tired.
And the scary thing about solidcancers so basically not like

(42:12):
the liquid blood cancers is thatthey have the capability once
they really do advance is toform this sort of fortress to
protect themselves like thisthink of the evil villain with
this massive castle with allthese like weapons and booby
traps in place.
So when, when the T cells come,they've got to chew their way
through this fortress and oncethey get inside the castle

(42:35):
there's toxic fumes.
It's a very hostile environmentthat basically, they just
effectively become dysfunctional.
So that's what we're trying todeal with.
We're trying to basically finda way to power up your immune
cells to be able to deal withcancer, because that's what they
normally do anyway, or precancerous cells.
They usually do a good job ofclearing it, even right now, as

(42:57):
we speak.
And, as I say, one of thesemethods is something called
immune checkpoint inhibitors,where basically one of the ways
that cancer cells and even thecells that so cancer cells can
manipulate cells like t-regs andthose were the cells that I
spoke to you about that, yeah,they basically cause immune

(43:17):
suppression.
They can manipulate t-regs andeven other immune suppressor
cells to come into the area andbasically protect them.
It's really scary, it's socrazy how that works.
So you know, you have yourimmune army coming to try and
hunt down cancer, but then theyencounter their buddies t-rex
and m2 macrophages and all theseother immune suppressor cells

(43:38):
that are basically there toswitch them off.

Speaker 1 (43:40):
So it's like dr evil's fembots he just screwed.

Speaker 3 (43:45):
They screw up austin powers honestly, basically, like
me and my friend, I should givehim a shout out, but we haven't
done it yet.
But we're planning to launchlike a, basically like a comic
strip on social media of as acomic but like cartoons of all
of this happening, because it'sjust crazy, it's like a war film
when you think about it.
So one of the ways with immunecheckpoint inhibitors is you're

(44:07):
basically blocking a couple ofthe ways that these suppressor
cells, or even cancer cells tryand switch off the anti-tumor
killer cells.
So by blocking those, thatmeans that weapon by the cancer
cells and immune suppressorcells can no longer work and

(44:28):
that helps out our killer cells.
The heroes of the storyactually do their job.
So that's what won the NobelPrize.
But what obviously we'reworking on where I work at the
moment in California, in LosAngeles, is taking sick patients
T cells out, as I said, andre-engineering them to be able

(44:49):
to go and hunt down the cancerand, yeah, re-infusing them and
just basically watching andhoping and waiting to see what
happens.
So we currently have threephase one clinical trials.
One of them is about to start,but the other two we are
targeting pancreatic, colorectal, non-small cell lung carcinoma,
ovarian cancer and mesothelioma.

(45:12):
So those are the main cancerswe're targeting at the moment.
A majority of our patients thatwe've dosed are pancreatic
cancer patients and I'm notallowed to share yet what's
happening, but definitely we'llbe releasing press releases at
some point soon just to give theupdate, because that first
clinical trial did begin.
I believe we've did those.

(45:33):
Our first patient in oh, this isembarrassing.
When was it?
April of 2023?
I want to say fairly sure.
I want to say 2023.
Made a fact check that eitherApril 2023 or April 2020.
Yeah, april 2023.
Sorry, I can't.
I just can't believe it'salready been two years since

(45:54):
I've been there it's likeyesterday since I joined.
So, yeah, we have been treatingthese patients and just, and
these patients that come intothese trials it sounds scary.
A lot of them really are endstage, like they've had maybe
not end stage because I don'twant.
Lot of them really are endstage Like they've had maybe not
end stage because I don't wantany of them here to get alarmed
or something.
But it's more, they've hadmultiple treatment lines that

(46:14):
maybe haven't worked or haven'tbeen able to keep them stable.
And that's why they enroll intothese phase one clinical trials
, because we're just trying togive them something else that we
think could work, because theother first line or second line
haven't necessarily worked forthem.

Speaker 1 (46:34):
That's.
It's just fascinating.
I literally could listen to youtalk about this for like days.
This is I've taken down likesome notes and I know I read a
paper not too long ago about theCAR T cells, that therapy like
they're.
I'm just you may you'll have tocorrect me if I'm wrong.
One of the advantages is thesesouped up cells like they stick
around in the body so they kindof are bodyguards for a while.
Am I on the right track there,or maybe that's a different

(46:56):
point.

Speaker 3 (46:56):
Yeah, this is really cool.
So we do have this concern.
That's the optimal situationwhere they stay there, because
sometimes we can't detect themin the blood after a while.
But maybe there's a lot aboutthis.
It because sometimes we can'tdetect them in the blood after a
while, but maybe there's a lotabout this.
It could be the reason whyyou're not detecting them in the
blood is because they're notactively circulating.
It's like when people say, oh,like you don't have immune

(47:16):
memory anymore because we can'tdetect antibodies in the blood,
and it's no, it's just theantibody.
They're not needed.
But the main cells are chillingin the like lymph nodes, for
example, or in the spleen.
They're just hanging out,they're on vacation, basically,
or they're just in the barrackswaiting for the call-ups.

Speaker 1 (47:34):
That's a better one.
That's a better analogy.
I like that.

Speaker 3 (47:37):
Exactly.
I say barracks.
I have no sort of armyterminology but I'm trying to
learn because I think that thearmy a lot of immunologists like
to refer to the immune systemas an army but more of waging
war when necessary, butpredominantly peacekeepers.
Ultimately they're trying tokeep balance and peace in your
body, because everything outsideis wanting to come into the

(47:57):
body, because our body is a verynice home.
It's like paradise.
But essentially so that's thething with CAR T cells.
What we're finding is, yes,that they can still be there and
they go and just chill in thelymph nodes and come back out
where necessary.
And there's really cool studieswith certain immunotherapies as
well, where they look atsomething called re-challenging.

(48:17):
So when we re-challenge, likemouse models for example, then
they're able to definitely clearthe cancers, for example, a lot
faster.
That's like the optimalsituation that you'll read in,
like these mouse papers, whereonce they're re-challenged,
they're able to just clearcancer so much faster.
Because the beauty of the immunesystem is it has memory.

(48:39):
Especially the adaptive immunearm has which are like the T
cells and B cells.
They have specific and highlyspecialized type of memory.
So that's the aim as well, isthat once they've seen it.
They can come back out and dotheir thing.
And I know, like with cancervaccine trials that's with
cancer vaccines they're reallyhoping to like trigger that

(48:59):
memory response.
But yeah, with CAR T cellsyou'd want them to always be
there and then they come backout where necessary.
So did you read?
Was this a blood cancer?
I'm guessing.

Speaker 1 (49:10):
I was and all of this is I'm not at your level of
expertise at all, but just forthe pod, my podcast a year ago
or so I related to my studentsas a video game analogy.
It's the immune system has amemory.
It's the more times you playSuper Mario you can get by the
levels faster.
And then, because you've soupedup these car T-cells, it's like
mario's not little mario, he'swhen mario gets the fire flower

(49:33):
and you can throw fireballs.
Not only does this immunesystem have memory, you're now,
you're souped up, kind of thingexactly, yeah, that's such a
good way of putting.

Speaker 3 (49:42):
Oh yeah, maybe I'll use, like the super mario kart
analogy.
I'll cite you, don't worry but,that's such a funny way of
thinking about it yeah, yougotta get the kids.

Speaker 1 (49:52):
You gotta get the kids engaged.

Speaker 3 (49:53):
Somehow they're sleepy in the morning, I tell
you yeah I could definitelyimagine and yeah, that's the
thing I think you can makescience or you can make
immunology like how can peoplenot be interested in this?

Speaker 1 (50:07):
It's so cool.

Speaker 3 (50:10):
They've evolved over millions and millions.
I think I was reading about thefirst ever phagocyte in life,
which is phagocyte means likeeating cell.
So these are like themacrophages, for example, that
just go around and chomp the badguys and then they have the
other, like processing in placeto be able to go wake up the
rest of the immune army.
But how the first phagocyteevolved and we're talking about

(50:33):
it's crazy.
We're talking about millionsand millions, hundreds of
millions of even fact check thisbillion years ago.
That part maybe needs to befact checked.
The point I'm trying to say isthis is prehistoric at this
point and all that's been like.
From that first phagocyte wehave now developed this
extremely intricate, compleximmune system that is so

(50:56):
powerful that it's it really isa double edged sword, because
it's so powerful that it cansave our lives, but also it can
kill us within minutes, you know, and that's what you have with
like cytokine storms that happen, or even anaphylaxis, which is
very scary when we're talkingabout serious allergic reactions
.
So you do have this equivalentof an intense atomic bomb that

(51:19):
could get detonated inside youby your immune cells if things
do go wrong.
That's I want people toappreciate.
I sound like an absolute not,but yeah, flip, I'm a scientist
obsessed in my field, but I justwant people to appreciate I
sound like an absolute nut, butyeah, flip, I'm a scientist
obsessed in my field, but I justwant people to appreciate right
, it's worship the immune system.
I want people to reallyappreciate the complexity and
just how it also deserves ourrespect.

(51:41):
And part of my page I'm wantingto segue, when I'm not getting
distracted by all the otherthings going on, is to make
people actually marvel and allat this complex immune system
that's trying to keep you alive,but also, if slightly out of
balance and if it gets so, ifit's slightly out of balance, it

(52:01):
will do.
Its number one priority, Ibelieve, is to get back to
balance.
That's what.
If you ask any immunologist,they have different theories
about what the key goal of theimmune system is.
My key theory is I have two keytheories.
It's one.
It's being keeping non selfquote, unquote, so not you out,

(52:21):
unless if it's like the goodsort of microbes that are inside
of you that are helping out andkeeping self in check, but also
keeping balance, maintainingbalance.
And if you tip that balance toofar to the point of no return.
That's when you get things likeautoimmunity or at least with
situations like allergies andfatal allergic reactions like

(52:44):
anaphylaxis, it's you havetrigger happy immune cells that
just can't distinguish likefriend or foe.
Essentially this, not this sortof non self that's passing by,
it's okay, it's safe, but itoverreacts and to the point that
, yeah, you can die.
So it is.
It sounds a bit of a morbidnote, but it is extremely

(53:05):
complicated and it's extremelyfascinating.
And whoever whoever says takethis pill, take this supplement,
it will reset everything andall your problems.

Speaker 1 (53:14):
And it's hun, it's not that simple, basically we
have the old facebook statusupdates with relationships.

Speaker 3 (53:22):
It's complicated yeah , oh my gosh, such as everything
it's.
And I think the people that aretrying to preach holistic, that
healthcare, maybe the peoplethat are the biggest corporates
of actually doing the opposite,which is approaching this with
the most reductionist approach,because it really just isn't
that easy, guys and I say thisbecause immunology, I think, is

(53:45):
one of the most complex fieldsin biology to understand, and
even scientists like me,immunologists like me, we're
constantly getting shocked atthe new things that are popping
up.
For example, the dogma for avery long time was that only the
adaptive immune system hasmemory.
No, now we're.
No, I say now.

(54:05):
Maybe people in the field for 10years have known that now the
innate immune system so yourfirst line actually has a type
of memory as well.
So we're just constantly andwe're learning that new cells
pop up, like it's just, it's socrazy, it's so fascinating,
there's so much that we don'tunderstand and are trying to
make sense of.
But that's why people like mein the immunotherapy space is

(54:28):
having the tools that we havenow we are trying to weaponize
and to keep up with the fightagainst things like autoimmunity
and cancer.
Once we infuse these patients,we learn new challenges.
The CAR T-cell realm has tonsof challenges, like, of course,
the blood cancer's CAR T-cellsare working beautifully.
However, they have come withtheir own challenges.

(54:50):
We have learned that even if weinfuse these CAR T cells to go
and destroy leukemia, theleukemic cells fight back.
They actually come up with newweapons oh my god, frustrating
but that's what's so incredibleis like we it's keeping
scientists on their toes becauseit's oh my gosh, this Luke.
So one one thing I can talkabout one mechanism is like

(55:12):
antigen escape and that's ifyou're reading that CAR T cell
paper maybe this came up.
But one of the reasons why CART cell therapy might fail is
because of this concept ofantigen escape.
So you engineer the CAR T cellsto be able to find a specific
antigen.
That's so for leukemia it willbe looking for particular B cell

(55:35):
antigen, because leukemia isnot T cell leukemia, b cell
leukemia.
One of the antigens is CD19,for example.
That's like a lot of B cellsexpress this particular antigen,
CD19.
When I say say antigen, justpretend.
It's like a little protein armjust sticking out the cell,
essentially.
But then what happens is wehave these cd19 car t cells and

(55:56):
it goes and it finds everythingthat has cd19.
So all these b cells absolutelyobliterates them.
Amazing news patients havecomplete response, no evidence
of cancer in the body, it's allgone.
And then suddenly, harrowinglylater, two months later, this
leukemia pops up again.
And you're like how?
And it turns out that afraction of those B cells

(56:21):
actually were not CD90, whendidn't have CD19, they had
another antigen up.
So that's the antigen escape.
They managed to escape therapybecause they actually had
another antigen that was beingexpressed and that the T cell
treatment missed them.

Speaker 1 (56:37):
And there's just so much 99% in the one left, and it
grew.

Speaker 3 (56:42):
It replicates and leukemia is so aggressive.
So you know it well, there'slike chronic.
It's just so much nuance.
There's like like the chronic,which is like the slowed burns,
but some of the acute leukemiasare very fast growing and deadly
.
It's keeping scientistsconstantly on their toes.
The biggest challenge withblood cancers is this antigen
escape fruit.

(57:02):
That's just one of the mainchallenges.
But then, as I say, with thesolid cancers, which is the
field that I'm in, it's how doyou deal with the fortress that
these solid tumors build?
So for some terminology we callit the tumor micro environment.
So the tumor micro environmentis very much been built up to

(57:24):
help sustain the cancer cellsand they really do make it a
very hostile, toxic environmentfor the immune cells that will
come and try and destroy it.
So how do we in the CAR T cellspace in solid cancers override
that toxic tumormicroenvironment?
So that's what we're trying tofocus on at the moment.

Speaker 1 (57:46):
Very cool.

Speaker 3 (57:47):
I could talk about this, for it's so sounds like
you need some kamikaze scottishhighlanders to take the first
charge against that fortressyeah, just screaming at them
with their kilts on but then youhave that risk of cytokine
storms happening oh, so I don'tknow if you can turn around and
come back at you.

(58:08):
It's more that they detonate.
They're like so amped up thatthey detonate all that, just
that image of like just sprayingwith machine gun bullets or
just throwing every possiblegrenade or bomb at them that you
end up.
The cancer cells are usuallynestled quite nicely in between

(58:30):
healthy tissue.
So then you cause this, likeyou cause this off tox off sorry
, off target toxicity where eventhe healthy tissue get
extremely damaged, and then youhave that cytokine storm where
basically all the other immunecells become amped up and it's
this positive feedback effectand eventually it can cause this

(58:50):
mass inflammation in the bodythat can kill patients.
We do have things in place now,protocols in place now as an
emergency when these patientsare getting treatment to be able
to deal with cytokine storms.
So I do want to if there'sanyone that's exploring cardi
cell therapy for themselves thatare listening, I do want to
just say that we now have toolsto be able to deal with cytokine

(59:12):
storms, but the point is we'retrying to find that balance
right, like we want to just goand throw absolutely everything
in the kitchen sink at thesecancer cells, but then no,
because you don't end up wantingto harm the patient in effect
as well with toxic side effects.
It's very complicated sideeffects.

Speaker 1 (59:33):
It's very complicated .
We end our show ends are in theinterview with a couple
questions about your pets.
We love it when our guestsshare a story about the pets
that they have or pets thatthey've known in their life.
I was wondering if you could dothat for us.

Speaker 3 (59:43):
Absolutely so.
I have two cats.
I've got two ragdoll mixes.
One's a ragdoll Himalayan andthe other one is a what we think
is a Siamese lynx point.
Basically they're brothers andwe found them in the shelter.
I can't believe cats thatflipping gorgeous were abandoned

(01:00:03):
in a shelter.
It's just criminal.
Actually, I don't want to saythat, I don't want to like judge
people's situations, but so oneof the cats is called shadow
facts.

Speaker 1 (01:00:17):
I 10 points.

Speaker 3 (01:00:17):
If you know the reference shadow facts oh,
that's gandalf's horse and lordof the rings, exactly gandalf's
oldest friend, basically theinspiration there was.
He was like a little shadow,just following me everywhere,
but he's so regal and somajestic and we're like it just
made sense, majestic to a point.
He like a little shadow, justfollowing me everywhere, but
he's so regal and so majestic,it just made sense.
Majestic to a point, he's alittle ragdoll.
So he does have, bless him, twobrain cells.
But and then we have the other.

(01:00:39):
One is called togepi.
Do you know the reference?
Maybe?

Speaker 1 (01:00:42):
oh, I've heard that you'll have to tell me.

Speaker 3 (01:00:44):
The name is very familiar, though yeah, so with
kids, that's the big clue,togepi, so it's a pokemon it's
got an eggshell right and it'sthe eggshell.

Speaker 1 (01:00:53):
It's like an egg.

Speaker 3 (01:00:55):
That's all I remember yeah, me and my partner were
like pokemon fans when we werekids and we wanted to try and
build in like well, we were fansof this anime called dragon
ball z Pokemon and Lord of theRings and Harry Potter.
Can we try and name pets afterthose particular key moments in

(01:01:15):
our lives?
So we called him Togepi,because he was this little
kitten that kept chirping and wewere laughing like he sounds
like the Pokemon, togepi, andwe're like, oh my God, that's
his name, togepi.
We have little Togepi inShadowfax and, yeah, it's so
funny because I've always wanteda ragdoll cat, like even before
they became popular.
I remembered watching homewardbound, which you must have seen

(01:01:37):
homeward bound absolutely andsassy.
I was obsessed with sassy as afive, six year old and I know
sassy is like a himalayan, butthat look, that himalayan,
ragdoll, siamese look, I justfound adorable.
So I always said I was going toget a cat that looked like that
and I kept bombarding mypartner on Instagram with all

(01:01:57):
these reels.
Of course, once you hitInstagram, here's you and your
algorithm just turns into that.
I think that's actually one ofthe ways I found you.
My algorithm ended up being allthese like cute cats and dogs
and then my partner was likebless him, famous.
Last words was like let's go toPetSmart, let's just humor

(01:02:18):
ourselves.
Little did he know that littleTogepi and Shadowfax were there
and I became obsessed andluckily, actually, the shelter
owners told us that.
So it's like a shelter, that'sa part, it's like a rescue,
that's a part of petsmart, yeah,and they said that apparently
they had like over 40 applicants, but they picked us.
So we're very happy about thatso yeah, we have our little boys

(01:02:41):
.
They're very cute, they're verynaughty, but they're well
behaved.
I know some cats can beabsolute demons, where they just
bite, scratch, hiss.
I don't even think our catsknow how to do that.
They're so cute.

Speaker 1 (01:02:54):
Yeah, our cat Ginger's a sweetheart too.
Yeah, so she's not a hisser ora biter.

Speaker 3 (01:03:01):
She seems to really put up with Bernoulli's nonsense
.
Oh my, she's a saint.

Speaker 1 (01:03:06):
Yeah, like when he was a puppy, it was, it was she.
We actually spoke to a vet.
I'm like what should we do?
And the vets?
You have to let them figure itout and the cat will eventually
fight back.
We're like, oh my god, it's notgoing good for her sometimes,
and then eventually she did, andthat's how they came to an
accord and they're best buds now.

Speaker 3 (01:03:23):
Yeah oh, that's amazing.
That's so good to hear.
When was the last gingermauling?

Speaker 1 (01:03:29):
Months ago, Months.
He just, yeah, Lily is obsessedwith her, so he'll trap her
occasionally, but he just licksher Like he'll just lick her.
So she's always soggy, Like yougo to pick her up and she's
just wet.
I'm like, oh gross.

Speaker 3 (01:03:42):
Oh, that's so cute.

Speaker 1 (01:03:52):
Togepi and shadow facts very cute.
Yeah, yeah, do they have offsetcolors?

Speaker 3 (01:03:55):
or does some of them have the black paws that
ragdolls might have?
So they both have.
They both look like typicalshadow facts.
Looks like a typical ragdollhimalayan mix, which is very
fluffy and has a black face,black paws oh, cute tail but
togepi is siamese lynx point, sohe has that lynx point on his
face.
He's very beautiful, looks likea siberian, but yeah, because

(01:04:15):
they got dumped at the sheltertogether.
But they're from differentlitters so we think that they
have one parent in common andthe other one might be, yeah,
like a different or maybe two,but yeah, they're different
letters.
So toga b is a little bityounger.
They're very young.
Their shadow fax is two and ahalf and toga b is turning two
in 20 days.

Speaker 1 (01:04:38):
Yeah, very cute.
Do you post your cat picpictures on your instagram
occasionally I'm I apologize ifI've missed them no, I haven't.

Speaker 3 (01:04:45):
I usually put them on my stories, but you know what?
I think I might start doingthat because I think it would be
fun to put them on my stories.
But you know what?

Speaker 1 (01:04:49):
I think I might start doing that because, I think it
would be fun to include them onmy grid as well we'll take my
wife and I'll take a look atyour stories to see if we can
get an eyeball on them.
But yeah, so much, I appreciateyou sharing your stories about
your cats.
That's adorable thank you, yeah, they're very cute uh, so we're
at the end of the chat.
Thank you, so so much for beingour guest today.
Doc, I mentioned you're onInstagram.

(01:05:10):
What's your handle there forpeople to find you?

Speaker 3 (01:05:12):
Yes, so it's doctor, but as in D-O-C-T-O-R dot, y-a-s
underscore, so doctoryasunderscore.
That's where you can find me onInstagram.

Speaker 1 (01:05:24):
Perfect, we'll make sure there's a link to you in
the show notes Anywhere else onsocial media or a website you'd
like to point people to not yet.

Speaker 3 (01:05:32):
There's things cooking up at the moment, but
yeah, for now, I'm, for now I'mjust on instagram.
So, yeah, that would be great.
Thank you so much decent.

Speaker 1 (01:05:41):
I so appreciate you giving up your time.
Thanks so much for chattingwith us.
As I said, I have about 17follow-up questions about the
immune system, but I want torespect your time and thanks
again for being a guest today.

Speaker 3 (01:05:53):
Of course.
Thank you so much.
This was so fun.

Speaker 1 (01:05:57):
That's it for this week's show.
Thanks for everybody comingback week after week to listen
to us.
A special thanks to our guest,dr Yas, and a big shout out to
our top tier patrons on thePodpack Plus plus.
If you want to support us orhear your name at the end of the
show, check out the link in ourshow notes.
Okay, chris, who are the topdogs?

Speaker 2 (01:06:16):
amelia fettig, re oda carol panel, jennifer challan,
linea janet karen cronister,vicky otero, christy walker,

(01:06:38):
sarah bram, wendy diane masonand luke helen chin elizabeth.
Thank you.
Debbie Anderson, sandy Breimer,mary Rader, bianca Hyde, andrew
Lin, brenda Clark, brianne Haas, peggy McKeel, polly Burge,
kathy Zerker, susan Wagner andLiz Button.

Speaker 1 (01:06:58):
For science, empathy and cuteness.