Description

PS! At 02:00, I incorrectly wrote MHCII instead of MHCI in the list of activation signals. I apologize for the typo, viewers!

This video covers the Cellular Immune Response, its effectors, and mechanisms of immunity against viruses.

All information in my immunology videos is sourced from:

• Book: Immunology, Eighth Edition by David Male, Jonathan Brostoff, David Roth, and Ivan Roitt
• Additional research: PubMed
• University lecture materials

Types of Immune Responses:

• Humoral Immune Response
• Cellular Immune Response
• Immunological Memory/T-cell Tolerance
• Hypersensitivity

Cellular Immune Response Targets:

• Virus-infected cells
• Oncogenic cells (Cancer cells)
• Transplanted cells

These are controlled through MHCI on their surface.

Effector Cells in Cellular Immunity:

• T-Cytotoxic Cells
• Natural Killer (NK) Cells
• Macrophages

T-Cytotoxic Lymphocyte Activation:

Requires three activation signals:

1. T-cell receptor (TCR) with CD8 and CD3 binds to MHCI.
2. CD28 – B7 interaction.
3. Cytokines (IFN-γ and IL-2) from Th1.

Once activated, T-cytotoxic cells express Fas Ligand (FasL), which binds to Fas on infected cells. They then release perforins and granzymes to induce apoptosis.

Natural Killer (NK) Cells:

Differentiate between healthy and infected cells based on surface receptors:

NK Cell Surface Receptors:

• Ly49: Binds to MHCI and sends a negative signal to prevent NK activation.
• NKR-P1: Recognizes proteins on infected cells and activates NK cells.
• Fas-L: Recognizes Fas-expressing sick cells.
• CD16: Binds to the Fc portion of antibodies, triggering antibody-dependent cytotoxicity.
• IL-2 receptor: Binds to IL-2 and activates NK cells.
• Surface markers: CD56+, CD16+, and CD2 (adhesion molecule).

Activated NK Cells Release:

• TNF-α: Activates endothelium and induces fever.
• IFN-γ: Enhances cytotoxicity, activates macrophages, and further stimulates NK cells.

Scenario of Cytotoxic Immune Response:

1. A virus infects a normal cell, making it a non-professional APC (does not express B7).
2. If a professional APC phagocytoses the infected cell, it presents viral fragments on MHC I and MHC II.
3. T-cytotoxic cell binds to MHC I via TCR-MHCI and CD28-B7.
4. Naïve Th0 binds to MHC II via TCR-MHCII, B7-CD28, and receives IL-12 → releases IL-2 (autocrine) → differentiates into Th1.
5. Effector Th1 releases IFN-γ and IL-2 to fully activate T-cytotoxic cells.
6. Effector T-cytotoxic cells express FasL, bind to Fas on infected cells, and release Granzyme B and Perforins to induce apoptosis.
7. Th1 activates macrophages via CD40L-CD40 and IFN-γ to eliminate remaining viral particles.

Immunity to Viruses:

• Adaptive Immune Response: Involves T-cells, resulting in immunological memory and antibody production.
• Innate Immune Factors:

General Factors:

• Viruses have specific cell receptors (tropism).
• Macrophages release inflammatory cytokines, inducing fever.
• Secretory factors: Feces, saliva, gastric juice.

Humoral Factors:

• Complement System (opsonization).
• Acute-phase proteins (Mannose Binding Lectin and C-Reactive Protein).

Cellular Factors:

• Phagocytosis
• Interferons

Interferon System:

Interferons (IFNs) are cytokines released in response to viral infection.

Types of Interferons:

• IFN-α: Released by leukocytes.
• IFN-β: Released by fibroblasts.
• IFN-γ: Released by immune cells.

Classification:

• Type 1 IFN (IFN-α, IFN-β):
  • Inhibits protein synthesis and DNA replication in virus-infected cells.
  • Increases MHCI expression on all cells.
  • Activates NK cells.
  • Stimulates T-helper and B-lymphocytes.
• Type 2 IFN (IFN-γ):
  • Reduces Th2 response.
  • Enhances Th1 response.
  • Activates NK cells and macrophages.
  • Differentiates B-cells into IgG-secreting plasma cells.

Antibodies Against Viruses:

• 1st week: IgM (Neutralizes circulating viruses).
• 2nd week: IgG (Targets circulating and extravascular viruses).
• IgA: Protects mucosal surfaces and prevents reinfection.

Summary:

When a cell is infected by a virus:

• It expresses Fas, which binds to FasL.
• Th1 activates macrophages to kill the infected cell.
• Antibodies may bind and neutralize the virus.
• NK cells may recognize and destroy the infected cell.
• The Complement System can also target the virus.

Transcript

Introduction
0:00
hello again and welcome to another video
0:01
in this video I’m gonna talk about the
0:03
mechanism of cellular immunity which is
0:05
one of the four main mechanism we have
0:07
in our body now we already looked at
0:09
human immune response and EEMA logical
0:11
memory now let’s go ahead and look at
0:13
what cellular immune response is so this
What Cellular Immune Response Is
0:16
is what you need to remember in terms of
0:18
cellular immune response
0:19
it’s that cellular immune response has
0:21
something to do with killing other cells
0:24
now which cells are their target first
0:27
one is obviously going to be cells that
0:29
have been infected with an intracellular
0:31
microorganism also could be oncogenic
0:34
cells or cancer cells and also can be
0:37
you know transplanted cells that are not
0:39
initially yours now why are all of these
0:42
three the target of your cellular immune
0:44
response the answer is the MHC one you
0:48
can think of MHC one it’s kind of a it
0:50
provides you a status update of the cell
0:53
and if the peptide that the cells
0:55
present on the MHC one it’s not
0:57
recognized as normal it’ll be killed so
1:00
a virus infected cell puts a fragment of
1:03
the virus on the MHC one so it’s killed
1:05
and oncogenic cell puts a fragment of
1:08
the mutated amino acid for example on
1:11
the MHC one and that is not normal and
1:14
then that’s why it’s killed and then a
1:16
transplanted cell of the other person’s
1:19
normal peptide is usually foreign for
1:22
the person receiving the organ
1:24
now what cells are responsible to clean
1:27
up the body from these cells first one
1:30
is obviously going to be T cytotoxic
1:32
lymphocytes natural killer cells are
1:34
like of warriors of cellular immune
1:36
response then we got macrophages these
1:38
guys are everywhere so let’s go through
1:41
the mechanism of each of these to see
1:44
how they work in the cellular immune
T-Cytotoxic Lymphocytes
1:46
response we can start with the T is a
1:48
toxic lymphocyte these guys are the kind
1:50
of t-cells that go hunt after sick cell
1:52
once they’re activated and just like any
1:55
other t-cells they need three activation
1:58
signals to activate so the first
2:00
activation signal so called t-cell
2:02
receptor notice that it has cd8 instead
2:05
of cd4 cd8 is going to dock on MHC one
2:10
multiple
2:11
and if you usually forget which MHC
2:13
binds to cd4 or cd8 the way I remember
2:17
it is that I always take the highest
2:19
with the lowest number so cd4 is the
2:22
lowest goes with the highest number of
2:24
MHC which is type 2 see the 8 is the
2:27
highest number of cd4 and cd8 so it goes
2:31
with the lowest MHC type so cd8 with MHC
2:36
1 and cd4 with MHC 2
2:38
so anyways t-cell receptor with cd8 and
2:42
it has also cd34 inducing a signal to
2:46
the cell after it binds so that is the
2:49
first signal it also expressed cd28 so
2:53
they combine to b7 for the second
2:55
activation signal the third activation
2:58
signal involves receiving interferon
3:01
gamma and interlocking to from an active
3:04
T helper cell 1 and that’s why I helper
3:07
cell 1 has some time has something to do
3:09
with a cytotoxicity as well not just
3:11
activated macrophages and activating
3:14
inflammatory response th 2 however has
3:17
more to do with B cell activation to get
3:19
antibodies so they’re more over to the
3:21
humoral immune response so T helper cell
3:25
1 helps cellular immune response when it
3:28
receives a signal it can finally
3:30
proliferate and differentiate into
3:32
effector T cell toxic cells so once T
3:35
cells has been activated they start
3:38
expressing FAS ligand what do they do
3:41
is that you know when cells are infected
3:43
they usually Express FAS so that when
3:47
the T cytotoxic cell binds is gonna kill
3:49
it by releasing preference with
3:51
perforates the membrane and then
3:54
Ransome’s which fragments their DNA so
3:56
that was mainly how the T cells work
3:59
I’ll show you a scenario later on how
4:02
this goes
4:02
but now let’s look at natural killer
Natural Killer Cells
4:05
cells these cells so they’re like the
4:08
policemen of your body they’re also able
4:11
to recognize unhealthy from healthy
4:12
cells and actually the fact that they
4:16
were able to do that by their surface
4:18
receptor which they already have on
4:20
their surface makes them a very
4:22
important part of the innate or natural
4:24
immunity
4:25
not the adaptive immunity all right keep
4:27
that in mind the natural killer cells
4:29
are a part of your innate immunity
4:31
because these guys are already able to
4:33
recognize six from from healthy cells
4:36
and I’ll show you how you know on the
4:38
surface of the natural killer so you’re
4:40
gonna have something called ly 49 and
4:42
you know normally cells Express MHC one
4:46
right all nucleated cells in your body
4:48
express MHC 1 and the ly 49 is going to
4:53
bind to it and once it binds to the MHC
4:57
1 is going to induce a negative signal
4:59
to the natural killer cell so that
5:01
natural killer cell doesn’t kill it
5:02
another surface receptor it has is
5:05
something called NK rp1 or natural
5:08
killer receptor p1 so you know where the
5:11
cell is virus infected and it’s and it
5:14
puts a little fragment of the virus on
5:16
the surface of the MHC one the thing is
5:19
natural killer cell cannot recognize the
5:22
peptide like a t-cell receptor can but
5:26
all the cells in your body expresses a
5:28
molecule on the surface which can be
5:31
recognized by the natural killer
5:33
receptor p1 and then that sends a
5:36
positive signal to the cell to kill the
5:38
cell now keep in mind that these
5:40
molecules on the surface of the cells
5:42
that bind to the natural killer cell
5:44
receptor p1 are usually always present
5:48
on the surface of your cell but once a
5:50
cell is infected it tends to reduce the
5:54
amount of MHC class 1 molecules on a
5:57
surface which means less ly 49 combined
6:01
and then again less negative signals to
6:04
the a cell so natural killers receptor
6:07
p1 takes over so that’s mainly how the
6:10
natural killer cell can differentiate
6:12
between healthy and and sick cells
6:14
it kills depending on how many MHC class
6:19
1 molecules a cell hasn’t surfaced and
6:21
so now what happens the natural killer
6:24
cell is going to release some granzymes
6:26
which is going to kill the cell
6:28
respectively another receptor that
6:31
natural killer cell is going to have is
6:33
the fast like in remember that one the
6:35
same one has in
6:36
Victor t-cell talks Excel remember when
6:39
a normal cell gets infected with an
6:42
intracellular microorganism is going to
6:44
express FAS natural killer cells can
6:48
recognize FAS by the FAS Ligon and then
6:51
is going to release perforins which
6:53
penetrates the membrane and then runs
6:55
arms which fragments the DNA to then
6:57
kill the cell we also have something
7:00
called CD 16 so you know in a normal
7:04
cell when it gets infected with a virus
7:06
more specifically when it gets infected
7:09
with a complex virus usually what
7:12
happens is that the viral nucleic acid
7:15
becomes integrated into the genome of
7:17
the host cell right what can happen is
7:20
that you know complex viruses gets out
7:23
from the cell through budding right it
7:25
just it just kind of fuses with the
7:27
membrane this goes out usually as it
7:30
prepares to go out through budding it
7:33
expresses some parts of the viral
7:36
peptides on the surface of the cell
7:39
during that time an antibody might bind
7:43
to the surface of the cell and what
7:46
happens then cd16 is going to bind the
7:50
FC region of the antibody and cd16
7:54
actually it binds specifically to the FC
7:57
region of of an IgG type antibody all
8:01
right so this this type of antibody
8:03
right here’s an IgG all right and then
8:06
after that it performs what is called an
8:08
antibody dependent cytotoxicity to kill
8:12
the cell all right so now we got ly 49
8:16
natural killer receptor p1 FAS lion and
8:19
CD 16 it also expresses interleukin-2
8:22
receptor which binds interlocking to and
8:26
gets activated remember I just show you
8:28
that the T helper cell one helps a T
8:31
cytotoxic cell activate by releasing
8:34
interlocking to interferon gamma here
8:36
you can see that T helper cell can also
8:38
activate natural killer cell by the help
8:40
of interlocking to other things it does
8:43
is that an active natural killer cell
8:45
releases tumor necrosis factor-alpha
8:47
we’ve already talked
8:50
how much about this one every time we
8:52
mentioned the macrophage because this
8:54
cytokine is able to help with the
8:57
inflammation process by you know
8:59
activating endothelial sites by
9:01
releasing antimicrobial proteins and
9:03
also expressing receptors to help cells
9:05
get to the information area tumor
9:09
necrotic factor is also a systemic
9:10
function that it causes fever by going
9:14
to the hypothalamus of the brain to
9:16
release prostaglandin e2 and cause fever
9:19
the natural killer cell can also release
9:21
interferon gamma I’ll talk more about
9:23
the interference at the end of this
9:26
video but interferon gamma has a lot of
9:29
functions it can help cytotoxicity by
9:32
activating more T helper cell one it can
9:35
activate other natural killer cells and
9:37
also macrophages and it can also
9:39
stimulate the b-cells into releasing rgg
9:42
so that’s those it also has an MHC one
9:47
it’s kind of logical because remember
9:49
MHC one is present on all nucleated
9:52
cells and natural killer cell also has a
9:54
nucleus or also has a messy one natural
9:57
killer cells also have MHC type 2
10:00
molecules it not really proven why they
10:03
have MHC class 2 molecules because they
10:05
are not antigen presenting cells that’s
10:08
why I haven’t included it but if you
10:10
read somewhere that they have MHC type 2
10:12
it might be true I’m not sure and so
10:15
another thing that’s really important is
10:16
that it has the surface marker CD 56 and
10:20
CD 16 and also has seen e2 which helps
10:24
with adhesion acidity 6 + CD 16 our
10:27
markers not CD 2 so that was everything
10:31
I had for the natural killer cells at
10:32
least now let’s play a scenario let’s
A General Scenario of Cellular Immunity
10:36
say this virus just infected the body
10:38
it’s either going to infect any type of
10:42
cells you have in your body or it’s
10:44
going to directly get eaten by an
10:46
antigen-presenting cell when a normal
10:49
cell gets infected in your body it may
10:52
present a part of the virus on an MHC
10:55
type 1 becoming what we call
10:57
non-professional antigen presenting cell
10:59
as it lacks be7 that’s why it’s not
11:02
professional
11:03
our professional antigen presenting
11:05
cells show b7 so if it infects a normal
11:09
cell the antigen presenting cell can’t
11:12
phagocyte the whole cell either way it’s
11:15
called a professional antigen presenting
11:17
cell because it can express the
11:19
important core stimulator receptor b7 as
11:22
well as presenting the peptide and MHC
11:25
class 1 or class 2 now remember at esata
11:28
toxic cell has TCR receptor which
11:31
includes the cd8 which binds to MHC
11:35
class 1 and c d3 which induces an
11:39
internal signal once it has bound this
11:42
is the first activation signal of the CT
11:45
cytotoxic cell the second signal is b7
11:48
binding the cd28 the third activation
11:52
signal comes from auntie T helper cell 1
11:54
so we need this professional antigen
11:56
presenting cell to kind of cross present
11:58
this peptide in this virus and a
12:01
dendritic cell is really really good at
12:03
cross presenting because this cell is
12:06
really big and has it has dendrites
12:08
which can extend to a lot of cells and
12:11
and activate many cells at the same time
12:14
so while it’s trying to activate the T
12:17
cytotoxic cell it’s also tried to
12:20
activate the naive T helper cell and it
12:23
does that through look it does that
12:25
through the T cell receptor MHC 2 and
12:27
through the b7 cd28 and it also are able
12:32
to differentiate it into a T helper cell
12:34
1 by releasing interlocking 12 it can
12:38
also receive interferon gamma from
12:40
natural killer cell 2 to get
12:42
differentiated now that cell is
12:44
activated after receiving the cytokines
12:46
it needs to grow to be able to divide
12:49
right and it does that through releasing
12:52
interlocking 2 which sits on its own
12:54
surface the process of releasing
12:56
cytokines which sit on your own surface
12:58
that process called out to clean so
13:01
they’re interacting to has an our
13:02
autocrine function so now it becomes a T
13:05
helper cell 1 and the T helper cell 1
13:08
can give the third activation signal
13:11
tivity site
13:12
Excel which is the interferon gamma and
13:14
interlocking to so that the cell can
13:17
differentiate and proliferate to an
13:21
active T cytotoxic cell which will
13:24
express FAS ligand now remember I told
13:28
you that the virus infected cells
13:30
Express FAS receptor right Nazira here
13:33
and after that he said toxic cells has
13:35
bound to it is going to release her
13:38
friends whispered the membrane and it’s
13:41
also going to release grenzen B which
13:43
has fragments the DNA and then kills the
13:46
cell but now we only have some
13:49
free-floating viruses you know the T
13:51
helper cell one it has another really
13:54
important function of expressing cd40
13:57
ligand which can bind to cd4 T on the
14:00
macrophage and then together with cd4
14:03
receiver Ligon and in different Gamma it
14:05
activates the macrophage into engulfing
14:08
they be remaining viruses the
14:10
free-floating viruses now immunity to
Immunity to Viruses
14:14
viruses can happen in two ways really
14:17
even adaptive or innate all of this I
14:21
just showed you involves T cells and
14:24
when T cells are involved then we shift
14:27
automatically to adaptive immune
14:29
response because remember an adaptive
14:31
immune response gives an immunological
14:33
memory of these viruses and also produce
14:37
antibodies against it since the T cells
14:40
are involved and I’ll talk about how
14:42
antibodies reactive viruses later in
14:44
this video
14:44
but the other main type of immunity
14:47
against viruses is going to be what we
14:50
call innate immune factors now there are
14:52
three factors of the innate immunity
14:55
that gives up a non-specific defense
14:58
the first one is general factors you
15:01
know viruses attacks host cells via
15:04
specific receptors right and this
15:06
partially determines which cell types
15:09
becomes infected this is called tropism
15:12
when they when the virus has specific
15:14
receptors on a host cell that it attacks
15:18
and if the host cell doesn’t really have
15:21
those receptors the virus can can’t
15:24
really infect it
15:26
that is what we call tropism we got
15:27
neurotropic viruses we get entero tropic
15:30
viruses so all of those are very
15:32
specific to what kind of cells they a
15:34
target so this factor is an example of
15:37
general factors we have for the innate
15:40
immune response against viruses
15:41
another way is you know macrophages it
15:45
can actually release inflammatory
15:46
cytokines once activated and they will
15:50
go to the hypothalamus of the brain and
15:52
cause fever reaction you know that when
15:54
the temperature increases it can make
15:56
harsher environment for viruses and
15:59
certain type of bacteria as well to live
16:01
in so that’s also a general factor of
16:04
the innate immune response against
16:05
viruses fever it could also be secretary
16:09
functions by thesis for example or
16:11
saliva those are also a general factors
16:14
the second type of innate immune factors
16:16
against viruses are humoral factors you
16:20
know the complement system are all the
16:22
time released by the liver the
16:24
complement system can also optimize the
16:26
bacteria and help fight against it as
16:28
well as interlocking six can also go to
16:30
the liver to cause it to release acute
16:33
phase proteins like C reactive proteins
16:35
or mannose binding lectin the mannose
16:38
binding lectin protein plays an
16:39
important role in humoral defense
16:42
against especially against the influenza
16:44
virus infection for example keep in mind
16:46
that the man is binding lectin is a part
16:48
of the complement system the last type
16:50
is called cellular factors and one of
16:53
them is phagocytosis you know
16:54
phagocytosis can happen when the type of
16:57
site just binds to the virus or even it
17:00
can happen directly the complement
17:01
system optimizes it or it can happen
17:03
directly if an antibody binds to it but
Interferons
17:07
another type of cellular factors are
17:10
what we call interference so let’s look
17:13
at how these work the interference play
17:15
a crucial factor in defense against
17:18
viruses and there are very important
17:20
signal proteins released by whole cells
17:23
often in response to several viruses so
17:27
there are also cytokines and there are
17:29
many interference types in our body but
17:32
I’ll mostly talk about these three types
17:34
in different alpha beta and gamma
17:36
interferon alpha is also called
17:40
leukocyte interferon because leukocytes
17:42
releases them and interferon beta is the
17:45
fibroblast interfering because
17:47
fibroblast releases them interferon
17:49
gamma is the immune interferon released
17:51
by several immune cells and we usually
17:54
group these interference though
17:56
according to the type of receptors
17:58
through which they bind interferon alpha
18:01
and beta are type 1 interference because
18:04
they bind to specific receptors called
18:06
interferon alpha beta receptor
18:07
interferon gamma are type 2 interference
18:11
usually activated by interlocking 12 so
18:14
let’s look at type 1 first and then look
18:17
at what type type 2 is so as the cell
18:19
gets infected by the virus the genes
18:22
that produce interfere in alpha and beta
18:24
are located on chromosome 9 right but
18:27
usually on normal cells these genes are
18:30
blocked but these infected cells you
18:32
know the virus that infected them
18:34
triggers interferon inducers to remove
18:38
this block right here completely and
18:40
when you remove this block it starts to
18:43
produce in different alpha and beta so
18:46
what did they do well for one thing once
18:48
the block is gone interfering alpha beta
18:50
will inhibit the protein synthesis and
18:53
the DNA thens synthesis in the in the
18:56
virus infected cell to stop the virus
18:58
from replicating then it will increase
19:01
the image see type 1 expression on all
19:05
the cells to protect them from from from
19:07
this mess they will also promote and
19:11
activate natural killer cell to kill it
19:14
interferon alpha beta will also activate
19:16
or actually stimulate T and B
19:19
lymphocytes so they can also help to
19:22
kill this virus and other infected cells
19:25
so at that is mostly type 1 interferon
19:28
type to interferon however remember
19:30
their interferon gamma and they could be
19:33
released by either T helper cell 1 T
19:36
cytotoxic cells and macrophages so you
19:39
know when an effector T helper cell one
19:41
releases interferon gamma
19:43
it’s going to reduce the amount of T
19:46
helper cell to we’re gonna have in the
19:47
body why is that it’s because the moment
19:51
the viral infection
19:52
habits in your body you need more
19:54
t-helper cell one that Teja Prasad – so
19:57
TL Prasad – is switched off and T helper
20:01
cell one the production increases they
20:04
also activate macrophages and natural
20:06
killer cells and also stimulate B cells
20:08
into differentiating to an IgG producing
20:11
plasma cell all of these is what the
20:15
interferon gamma does it’s released also
20:18
by an active natural killer cell and
20:20
also of an active a T cytotoxic cell now
20:23
you see these IgG immunoglobulins
20:26
remember I told you that the adaptive
20:28
immunity against viruses also casts
20:31
antibody to get released these are
20:34
produced by plasma cells and in the
20:36
first week of infection IgM is going to
20:40
be circulated around your bloodstream to
20:42
neutralize the circulating virus and I
20:44
remember the humoral immune response
20:46
when I told you that
20:47
IgM is going to be the fastest produced
20:50
antibodies because it’s produced without
20:53
the help of t-cells but then in the
20:55
during the second week after you know
20:57
all the T cells have reacted and b-cells
21:00
reacted and all that
21:02
IgG is going to be released so that’s
21:04
why rgg takes a little more time and
21:06
they are going to circulate around your
21:09
body and look for viruses and they can
21:11
also catch extravascular viruses even
21:13
when the viruses are inside the cell as
21:15
a result you can also find i GA e on the
21:19
mucosal surface to protect against
21:20
reinfection so what type of acquired
21:24
immunity do we have against viruses
21:27
there are a lifelong immunity like mises
21:30
measles for example we also have low
21:33
level immunity those are usually chronic
21:35
viral infections or we can have no
21:38
immune response those are slow viral
21:41
infections like appliance for example
21:43
those are just proteins
Summary
21:45
now let’s sum up a virus infected cell
21:49
can show a fast
21:50
FAS for a t cytotoxic t killed by
21:53
releasing
21:54
preference and granzin be another way is
21:58
by T helper cell one activated
22:01
macrophage with the help of cd4 TL and
22:04
interferon gamma which will then
22:06
phagocyte the virus natural killer cell
22:10
can kill it by either surface receptors
22:12
and even antibodies can up sighs the
22:15
cell and cause other cells to bind to
22:17
the antibody and kill it or even it may
22:20
activate the classical pathway of the
22:22
complement system another way is that if
22:25
you have a free-floating virus
22:26
antibodies can also optimize it as well
22:29
so that was everything I had for the
22:32
cellular immunity lastly let’s look at
22:35
how hypersensitivity goes