Description

This video is about Hypersensitivity and its classification.

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

Hypersensitivity: Excessive Immune Response

Hypersensitivity reactions occur when the immune system responds excessively to an antigen, leading to tissue damage.

Coombs and Gell Classification of Hypersensitivity:

• Type 1: Immediate Hypersensitivity (IgE-mediated)
• Type 2: Antibody-Mediated Hypersensitivity
• Type 3: Immune Complex Disease
• Type 4: Cell-Mediated Reactions

Type 1 Hypersensitivity: IgE-Mediated Hypersensitivity

Occurs when IgE antibodies on mast cells trigger anaphylactic shock.

Factors that Induce Allergy:

• Pollen
• Inhaled particles (dust, pet dander, mold spores)
• Milk, fish, nuts
• Direct skin contact allergens

Genetic predisposition plays a role in allergic hypersensitivity.

Development of Type 1 Hypersensitivity:

1. First exposure: Inhaled pollen enters the body.
2. Phagocytosis: Langerhans cells (or other APCs) phagocytose pollen and travel to the lymph node via afferent lymphatic vessels.
3. Sensitization Stage (in the lymph node):
   • APCs present the antigen on MHCII to a naive T-helper cell.
   • Three activation signals occur: TCR-MHCII, CD28-B7, and IL-4.
   • IL-2 promotes Th0 proliferation into effector Th2 cells.
   • B-cells that bind pollen undergo receptor-mediated endocytosis and interact with Th2, leading to IgE production.
4. Sensitization phase duration: 6 months to 5 years.
5. Second exposure: Pollen binds to IgE antibodies on mast cells.
6. Mast cell degranulation: Histamine is released, leading to:
   • Vasodilation
   • Increased capillary permeability
   • Bronchoconstriction
   • Secretion of IL-5 and TNF-α

Type 2 Hypersensitivity: Antibody-Mediated Immune Response

Involves IgG or IgM antibodies targeting cell surface antigens.

Possible Causes:

• Viral Budding: Some viruses place their proteins on the host cell surface, leading to antibody recognition.
• Blood Transfusion Reactions: Mismatched ABO blood types can trigger immune destruction of red blood cells.
• Drug Allergies: Some drugs can bind to cell surfaces, making them targets for antibodies.
• Autoimmune Reactions: T-cell tolerance failure can lead to autoimmune diseases.

Mechanism:

1. Antibodies bind to surface antigens.
2. Activation of the Complement System:
   • MAC formation leads to cell lysis.
   • C3b opsonization allows phagocytes to bind via C3b receptors.
3. Neutrophils and NK cells recognize and destroy the antibody-coated cells.

Type 3 Hypersensitivity: Immune Complex Disease

Immune complexes (antigen-antibody complexes) form and deposit in tissues, causing inflammation.

Pathophysiology:

• Normally, immune complexes are cleared by the liver and spleen.
• If they persist, they can become trapped in vessel walls, activating the complement system.
• Neutrophils, basophils, and mast cells respond, leading to inflammation (Arthus Reaction).
• Platelets aggregate, further worsening the reaction.

Examples:

• Serum Sickness: If bitten by a venomous snake, injecting anti-venom (pre-formed antibodies) can cause immune complex formation.
• Systemic Lupus Erythematosus (SLE): Persistent immune complexes cause chronic inflammation.

Type 4 Hypersensitivity: Cell-Mediated (Delayed-Type Hypersensitivity)

Involves Th1 and T-cytotoxic (T-cyt) cells triggering local inflammation.

Example: Tuberculin Skin Test (Mantoux Test)

1. Injection: Tuberculin is injected into the skin.
2. Phagocytosis: Macrophages or Langerhans cells engulf tuberculin.
3. Antigen Presentation: APCs travel to the lymph node and present tuberculin on:
   • MHCII to naive Th0 cells.
   • MHCI to naive T-cytotoxic cells.
4. Th1 Activation:
   • Three activation signals occur.
   • IL-2 helps differentiation into effector Th1.
5. T-cyt Activation:
   • IL-2 and IFN-γ promote differentiation into effector T-cytotoxic cells.
   • Effector T-cyt expresses FasL, which binds Fas on infected cells.
   • Releases perforins and granzymes, causing apoptosis.
6. Second exposure:
   • Phagocytes activate effector Th1 and T-cytotoxic cells.
   • Th1 releases IFN-γ to activate macrophages.
   • Macrophages release inflammatory cytokines (IL-1, IL-6, TNF-α).

Other Type 4 Hypersensitivity Examples:

• Contact dermatitis (e.g., poison ivy, nickel allergy).
• Granuloma formation in tuberculosis.
• Graft rejection.

Transcript

Introduction
0:00
hello again this video is going to be
0:01
about hypersensitivity imagine there’s
0:04
the sky which gets infected by bacteria
0:05
or virus the adaptive immune response
0:08
provides a specific protection against
0:11
infections with bacteria viruses
0:13
parasites or even fungi some immune
0:16
responses however give rise to an
0:18
excessive or inappropriate reaction this
0:21
is usually referred to as
0:22
hypersensitivity the term
0:24
hypersensitivity evolved about 100 years
0:27
ago where they would sensitize an animal
0:30
with antigens like that so the animal
0:33
would produce antibodies against an
0:35
antigen then they would expose this pre
0:38
senseless animal with a systemic antigen
0:41
the resulting outcome was called
0:43
anaphylaxis and became the term that
0:45
described the immediate hypersensitivity
0:47
reaction Coombs and gel in 1963 came up
0:52
with a way to classify the different
0:54
types of hypersensitivity we have they
0:57
came up with four different types type
0:59
one was termed immediate
1:01
hypersensitivity reaction and is
1:03
characterized by the production of IgE
1:06
antibodies against foreign proteins that
1:08
are commonly present in the environment
1:09
like Pollan for example these usually
1:12
sit on mast cells type 2 was called
1:16
antibody mediated hypersensitivity
1:18
responses and that occurs when IgM more
1:21
IgG antibodies are produced taking
1:23
surface antigens on the cells of the
1:26
body
1:26
type 3 is immune complex diseases and
1:29
that involves formation of immune
1:32
complex in the industry regulation and
1:34
then the last one is type 4 and that one
1:36
was called cell mediated reactions where
1:39
T says toxic cell and T helper cell 1
1:42
at the main cause of that so now let’s
1:45
start with type 1 and then work our way
1:47
down from there so type 1
Type 1 – Immediate Hypersensitivity Responses
1:49
hypersensitivity as mentioned is also
1:51
called IgE mediated hypersensitivity
1:54
since reaction typically rely on IgE
1:57
antibody which is nearly always gonna be
2:00
found on the surface of mast cells or
2:02
basophils even which in terms make sense
2:06
since the typical reactions of type 1
2:08
hypersensitivity
2:09
leads to an effect
2:11
shock caused by an activation of these
2:13
cells this is the most common type of
2:16
allergy so there are a couple of ways to
2:18
induce a type 1 hypersensitivity
2:20
reaction one of them is inhaling it
2:23
could be different types of pollen for
2:25
example or even particles from animals
2:27
for example other include foods like
2:30
fish or dreams like milk or even the
2:33
physical contact could induce an
2:35
allergic reaction having an IgE mediated
2:38
reaction against the things that
2:40
normally don’t trigger the immune
2:42
response now having an IgE mediated
2:44
reaction against things that normally
2:48
don’t trigger the immune system it’s
2:50
usually mostly because that person has a
2:52
genetic predisposition towards
2:55
developing a certain allergic
2:56
hypersensitivity so let’s see what
2:58
happens so let’s say there’s a person
3:01
that has never been exposed to Poland
3:04
before right but that person has a
3:06
genetic predisposition towards
3:09
developing an allergic hyper sensitivity
3:11
towards pollen so let’s say this person
3:14
breathed in a little bit of pollen for
3:16
the first time now let’s take a look at
3:19
the surface of the lungs of this person
3:21
to see what happens beneath the surface
3:23
there are going to be cells like
3:25
dendritic cells or macrophages now as
3:28
the person breathe in poem the antigen
3:31
presenting cells will find it foreign
3:33
and phagocytose it and then presented an
3:36
MHC class 2 molecule and then it will go
3:40
to the lymph nodes through the efferent
3:42
lymph vessels and remember the efferent
3:44
lymph vessels is gonna drain the
3:46
interstitial fluid from different
3:48
tissues in your body right so both the
3:52
poem and the dendritic cell is going to
3:54
go through the efferent lymph vessels to
3:57
the lymph node and the lymph node looks
3:59
like this right or looks sort of like
4:01
this it’s gonna have
4:03
efferent lymphatic vessels and efferent
4:05
thematic vessels it’s also going to have
4:07
medulla it’s going to have the power
4:09
cortex or the T cell zone where the T
4:12
cells are and in outer cortex where the
4:15
B cells are which are composed of
4:17
primary and secondary follicle now when
4:19
they reach length what happens remember
4:22
that the body reacts to
4:24
paalam the same way as it reacts to any
4:27
type of microorganisms so it’s going to
4:29
produce antibodies against that pole so
4:33
we need T helper cell to to make
4:35
antibodies right so the professional
4:37
antigen presenting cell will present the
4:39
phone to a naive T helper cell using MSE
4:42
– which will bind to a t-cell receptor
4:45
where the cd4 will dock to the MHC 2
4:49
molecule which will cause the cd3 to
4:53
induce a signal internally inside the
4:56
cell this complex of TCR MHC 2 is the
5:00
first activation signal to activate the
5:03
naive T helper cell now remember there
5:05
are three activation signals required to
5:08
activate the or to differentiate the
5:11
naive T helper cell all right
5:12
the second activation signal is through
5:15
cd28 and b7 molecule and then the third
5:19
thing knows when it receives into the
5:21
kin for from other T helper 2 cells or
5:24
mast cells or even buzz opiates can also
5:26
release interleukin 4 and then it will
5:29
release interacting – which will bind to
5:32
its own surface this is called an
5:33
autocrine function and this causes the
5:36
cell to proliferate and differentiate
5:38
into effector T helper cell 2 which will
5:42
express cd40 ligand and will also
5:44
release interlockings
5:46
interlock intent suppresses the
5:48
activation of T helper cell 1 remember
5:51
that T helper cell – and he helped set
5:52
one kind of works against each other one
5:56
of them proliferate the other one is
5:58
suppressed interlocking four five and
6:01
six acts on B cells and I’ll show you
6:03
how in a second so while this is
6:06
happening a naive B cell that happens to
6:09
have a receptor on surface that matches
6:12
the poem undergoes a b-cell receptor
6:15
mediated endocytosis and expresses it on
6:18
MHC type 2 right and then it’s going to
6:22
travel to the secondary follicle and
6:24
then it’s going to go as close to the
6:27
para cortex as possible to get some help
6:30
by the T helper cell to to proliferate
6:32
and differentiate you can find it going
6:35
into the actual Parker Texas
6:36
well in some cases so now the naive
6:40
b-cell expresses the poll on MHC type 2
6:43
right it expresses it to our th2 cell
6:47
that initially got activated by an
6:49
antigen-presenting cell that presented
6:51
the same type of pollen now keep in mind
6:54
that D cells are also professional
6:56
antigen presenting cells and can help
6:59
differentiate naive T helper cells as
7:01
well so now remember in the lymph node
7:04
cd40 ligand binds to cd4 T this is the
7:08
second activation signal for the B cell
7:10
the first being when the B cell actually
7:12
binds to the pole so when the B cell
7:15
binds the poll has the first activation
7:16
signal when the cd4 t binds to see the
7:19
for ligand as the second activation
7:20
signal the third activation signal for
7:23
the B sub to start proliferating that is
7:26
receiving intelligence from the T helper
7:28
cells and the T helper cell can release
7:31
interlocking for release in 2005 in 11:6
7:34
and ended up in ten or even receive
7:37
interlocking two or in different gamma
7:39
from th one cell to differentiate into a
7:42
plasma cell that secretes antibodies and
7:44
two memory cells now keep in mind that
7:47
it doesn’t receive all of those
7:49
interactions together it actually
7:51
receives a specific interlocking
7:53
according to what antibodies we need so
7:57
let’s say we need more IgA for instance
8:00
then we would receive more interlocking
8:02
v if we need AGG we would get in
8:04
different gamma or even interlocking for
8:07
King gets us a subtype of IgG as well
8:09
our GM is produced without the help of T
8:12
cells and our Gd as well since they are
8:14
part of b cell development but if we
8:17
need a GE remember IgE is going to be a
8:20
part of the type 1 hypersensitivity we
8:24
get them by receiving interlocking for
8:26
and they have a really high affinity to
8:29
sit on the surface of mast cells and
8:31
basophils
8:32
this stage of hypersensitivity is called
8:35
a sensitization stage and that stage is
8:38
when you actually produce the antibodies
8:41
right so now this guy is sensitized
8:44
right that means we’ve made antibodies
8:48
against
8:48
the poll on this stage of being
8:51
sensitized usually last from six months
8:54
to five years meaning that it is
8:57
possible to lose the antibodies we
8:59
actually produced for the problem if we
9:02
don’t get exposed to pole
9:04
within that period within six months to
9:06
five years and after that after the
9:09
period we’re done with sensitization
9:11
stage if we have walked around for a
9:13
long time without being exposed to
9:15
pollen we will lose the antibodies and
9:17
then we’ll go back to not being
9:18
sensitized and then after that once
9:21
you’re exposed to pollen again you will
9:24
then go through the sensitization stage
9:26
again so that’s mainly how a
9:28
sensitization functions so now the
9:31
second stage is the second exposure
9:33
remember we will already have mast cells
9:35
with IgE type antibodies against pollen
9:38
right now when this person breathes in
9:41
Poland again usually requires more than
9:44
this one it triggers the mast cells into
9:46
releasing and mediators like histamine
9:49
which causes vasodilation for example
9:51
and also increases the permeability for
9:54
water and cells to go out from from the
9:57
blood to the interstellar space in the
9:59
area where the mast cells are this is
10:02
usually good if you have an infection of
10:04
certain type of micro organisms but when
10:07
in this case when the case is only
10:09
pollen which really isn’t that dangerous
10:11
for the body it’s very bad because it
10:14
causes unnecessary damage to your
10:16
tissues what also could happen is that
10:18
it increases the permeability of blood
10:20
vessels and that causes more water to
10:22
flow in and you get more interstitial
10:24
fluid than normal and that could cause
10:27
edema for example it also causes
10:29
bronchial constriction so the person
10:31
can’t really breathe too well other
10:34
mediators are heparin and trypsin they
10:36
have a sort of the same function also it
10:39
secretes out interleukin 5 which
10:41
activates a Arsenal fails and get IgA
10:44
and also to Myrna Craig factory which
10:47
promotes inflammation and cause fever so
10:50
that’s mostly how type 1
10:53
hypersensitivity works it it’s called an
10:56
immediate hypersensitive response
10:58
because once you’re sensitized and you
11:01
breathe in that
11:02
you breathe in Poland you see all of
11:04
those things that happen they happen
11:06
instantly because you already have
11:08
antibodies against Paul so that’s type
Type 2 – Antibody Mediated Hypersensitivity Responses
11:11
one now over to type two type two is
11:14
what we call antibody mediated immune
11:17
response against antigens on the surface
11:19
of your cells and they’re either IgM or
11:22
IgG now remember normally you don’t
11:25
really have that because you just don’t
11:28
want your body attacking your own cells
11:30
and there are possible reasons for this
11:33
one of them is if you’re infected by
11:36
complex viruses imagine a cell right and
11:40
the cell gets infected by a complex
11:43
virus and complex viruses usually gets
11:46
out from the set once they replicate
11:48
they usually get out of the cell by what
11:51
we call viral budding right so when they
11:54
integrate their own DNA into our own
11:57
genome to produce their proteins and
12:01
these proteins are usually attached on
12:03
the surface of the cell and the membrane
12:05
to prepare for viral budding when they
12:07
when the virus actually fuses with the
12:09
cell membrane to get out and as a result
12:12
from that you tend to have antigens on
12:15
the surfaces cell yet what can happen is
12:17
that antibodies can can actually form a
12:21
complex on the surface of the cell and
12:23
what they have now now we have type 2
12:26
antibody mediated hypersensitive
12:27
response because you see antibodies on
12:30
the surface of the cell other possible
12:33
reasons are draw colleges if you take
12:35
and it’s also drug penicillin for
12:37
example these drugs has a tendency to
12:41
also sit on the surface of the cell if
12:44
that happens and you’re allergic to
12:46
drugs
12:46
you also get secondary immune response
12:48
other types are transfusion reaction so
12:52
imagine a person a having blood type A
12:54
meaning if they have a antigens on the
12:58
surface of the red blood cells and
12:59
another person a person B has a blood
13:03
type B which has B antigens on the
13:05
surface of the red blood cells but they
13:07
also have
13:09
and tea a so antibodies against a
13:11
antigens so if person B is in need of
13:15
blood and for some reason receives blood
13:17
from person a what then is gonna happen
13:20
that an ta is going to react to the
13:23
person a red blood cells and now we also
13:26
have type 2 hypersensitivity the fourth
13:29
way is the apt to immune reactions for
13:33
example where we need to look at t-cell
13:36
tolerance T cells get controlled so that
13:40
they don’t react to our own cells and T
13:43
cell tolerance happens to places it
13:45
could be central tolerance that happens
13:47
in the thymus where immature T cells are
13:50
exposed to self antigen and is killed if
13:54
they do react to our own antigen but
13:57
this process isn’t perfect though and
13:58
some can actually escape to the
14:00
periphery today to the secondary
14:02
lymphoid organs where the peripheral
14:05
tolerance happens here T regulatory
14:07
cells and direct inactivation happen if
14:10
it escapes from here to we then get out
14:13
to human disease now what could happen
14:16
if an antibody binds to the surface of a
14:18
cell one thing is that the classical
14:21
pathway could happen where the c1 binds
14:23
to the FC part of the antibody remember
14:25
this these are usually IgG type
14:27
antibodies now c1 can cleave c4 into c4
14:32
BC for a and C one can cleave C to the C
14:36
to B and C to a and these to C 2 C 4 BC
14:40
to be work as a c3 convertase which
14:43
cleaves c3 into c through a and C
14:47
through be either it binds to the t3
14:49
convertase and come c5 convertase or it
14:52
binds to the surface of the cell itself
14:54
and and works in absanon now c5 can get
14:58
cleaved now what can happen
15:00
you see those c2 AAC for a c3 and c5 a
15:04
these guys worked as chemotaxis and
15:07
remember these had tax in their name so
15:10
they lead the way for white blood cells
15:12
to come this is a neutral field for
15:13
example they can bind to the c3 be that
15:18
works at an optional
15:19
and also or they can bind to the
15:22
antibody directed the complement system
15:24
never happened
15:25
now this neutrophil can either take a
15:27
site this cell or if it if the cell is
15:30
too big or if it can’t focus at the cell
15:32
it gets frustrated and releases
15:35
mediators like proteases and peroxidase
15:37
to kill the cell
15:38
another way is you know c5 b c6 can bind
15:42
t7 c8 and c9 and now we get a structure
15:46
called membrane attack complex and that
15:49
can can make a lot of holes on the cell
15:51
that ruins the environ ternal
15:55
environment of the cell and that can
15:56
cause the cell to die other things that
16:00
could happen is you know instead of a
16:02
neutrophil maybe a a natural killer cell
16:05
can come natural killer cell also have
16:07
receptor for c3 B and also receptors for
16:10
the FC region of an IgG you know they
16:12
can also release you know granzymes and
16:15
and preference to kill the cell
16:17
so you see type 2 antibody mediated
16:20
hypersensitivity response is is more or
16:24
less the it targets your own cells by a
16:26
lot of reasons
16:28
so that was mainly type 2
16:30
hypersensitivity type 3 is what we call
Type 3 – Immune Complex Diseases
16:33
immune complex disease where immune
16:36
complexes like these are formed in our
16:39
blood
16:39
notice type 2 and type 3 are exactly the
16:43
same the only difference is is that type
16:45
2 is related to antibodies that are
16:47
bound on the server of cells type 3
16:51
however is with antibodies bind to
16:53
free-floating antigens usually in the
16:56
blood so if it’s in the blood it usually
16:59
causes a systemic response or it could
17:01
be local if you in your lungs for
17:04
example so let’s say this is a blood
17:06
vessel right with some immune complexes
17:08
in it normally your liver and spleen
17:11
gets rid of these once they arrive to
17:13
either one of them but some may never
17:16
even reach them some may may get stuck
17:18
on the walls of the blood vessel right
17:21
somewhat like like this for example now
17:24
what can happen the complement system
17:26
can bind just like shortly before and
17:30
they can release chemotaxis like
17:32
neutrophil
17:33
could could bind and release local
17:36
granules that cause tissue damage and
17:38
local inflammation and that local
17:41
inflammation Peaks usually in 6 to 12
17:44
hours even bakso fields can even bind
17:47
and they can release granules and
17:49
vasoactive amines and even platelets can
17:52
come along and they can aggregate as a
17:54
result from it I don’t know if you’re
17:55
familiar with the physiology of
17:57
platelets but they usually tend to
17:59
aggregate on rough areas and that’s
18:02
exactly what the immune complexes are
18:04
once they’re stuck so that’s why they
18:07
aggregate on them they could even
18:09
activate mast cells in area that can
18:11
release histamine all of this mess right
18:14
here is termed archers reaction by
18:17
nicholas maurice arthur who discovered
18:20
all of this for the type 3
18:22
hypersensitivity the other type of
18:24
reaction of type 3 hypersensitivity is
18:27
well called serum sickness disease so
18:30
imagine you’re out walking and then
18:31
unfortunately a snake comes in by to you
18:33
and it secretes its venom into your
18:36
bloodstream and if you’re quick enough
18:38
and reach the closest healthcare and
18:40
they luckily has an antidote they can
18:44
inject the anti snake venom which you’ll
18:46
have new blood stream so now immune cup
18:49
free immune complexes or are also for in
18:52
your blood so that is also type 3
18:54
hypersensitivity immune complex disease
18:57
so that was type 3 now last one is type
Type 4 – Cell Mediated Reactions
19:01
4 hypersensitivity also known as cell
19:04
mediated reactions where T helper cell 1
19:07
and T set toxic cell are involved mainly
19:10
and can cause a lot of inflammation in
19:13
the skin one famous example is the
19:16
tuberculin skin test or the among dose
19:18
test this test is to check if you’ve
19:22
been infected with the Mycobacterium
19:24
tuberculosis before and these bacterias
19:27
release a protein called tuberculin and
19:30
if we’ve been infected with this
19:32
bacteria before we should react
19:35
tuberculin fast so let’s say you’ve
19:38
never been infected with this bacteria
19:40
right where’s where sensitization stage
19:43
and the second exposure still still
19:44
counts
19:45
this test start off by injecting a
19:48
Tibetan into the skin Langerhans cells
19:51
which is a skin dendritic cell will flag
19:54
aside it and then run off to your
19:56
afferent lymphatic vessels so now
19:59
Langerhans cells has phagocytosed the
20:02
tobacco Lin right and then it’s going to
20:05
present it on an MHC type 2 molecule and
20:08
then it’s going to travel to the lymph
20:10
node to present it to a naive T helper
20:12
cell a naive T helper cells gonna use
20:15
its cd4 to to kind of dock to the MHC
20:18
type 2 molecule and then C D 3 which is
20:21
also a part of the T cell receptor is
20:23
going to send a positive signal to the
20:25
cell nucleus internally so that is the
20:28
first signal to activate in
20:30
differentiate the T helper cell the
20:32
second signals between b7 and cd28
20:35
Langerhans cells only expresses b7 once
20:38
it’s reached the lymph node keep that in
20:40
mind and then it’s going to release
20:43
interlocking 12 that’s a third signal
20:45
remember look at the name it’s called
20:46
cell mediated reaction that’s why we
20:50
need T helper cell 1 because T helper
20:52
cell 1 help activate macrophages to
20:54
induce inflammation but they also help
20:57
activate T cytotoxic cell which is a
21:00
part of the cell marriage reactions
21:02
alright so we need T helper cell 1 so
21:05
now after interlocking 12 has bound to
21:08
the surface of the 90 helper cell it’s
21:10
going to release interlocking 2 which is
21:13
going to bind on its own surface that is
21:16
called an outer cream function and
21:17
that’s going to help it grow and
21:19
differentiate and undergo clonal
21:22
expansion so now the th1 cell it’s an
21:25
inflammatory t-cell that activates
21:27
macrophages by releasing interferon
21:30
gamma which also causes production of
21:33
IgG and also decreases the th to
21:36
production to focus more on the th one
21:38
it’s also going to release interleukin 2
21:41
which helps B and T cells to grow so a
21:46
dendritic cell is very good at cross
21:48
presentation keep that in mind because
21:50
then drilling cells are very big and
21:52
they have these processes which can
21:54
reach to a lot of cells and activate
21:57
them as Immelt
21:58
so that’s what it usually does it’s also
22:01
going to present the a part of the table
22:04
clean on the MHC class 1 which is going
22:07
to attach to the tea set of toxic t-cell
22:11
receptor because remember they have cd8
22:14
they don’t have cd4 and cd8 helps dock
22:17
to the MHC class 1 model so that’s also
22:21
going to induce a signal to the cd3
22:24
that’s the first activation signal the
22:26
second activation signal is b7 and cd28
22:29
and then the effector T helper cell 1 is
22:33
going to release interacting 2 and
22:35
interferon gamma they both are going to
22:37
help the T cytotoxic cell become an
22:40
effector T cell toxic cell which is
22:43
going to express what is called fast
22:45
ligands and you know any type of cells
22:48
that are infected is going to express
22:50
FAS and that’s exactly why the T
22:54
cytotoxic cell has FAS ligand because
22:57
it’s gonna bind to FAS the receptor and
23:00
in and release preference which pervades
23:03
the the membrane of the cell and
23:04
granzymes which usually fragments the
23:07
DNA of the cell and causes it to die now
23:11
remember that th 1 and T so toxic cells
23:14
also becomes memory cells and memory
23:17
cells are the ones that can give you a
23:20
reaction really fast right so now we’ve
23:23
done with the sensitization stage and if
23:27
we get exposed to tobacco again after
23:30
some time about 28 days for example so
23:34
it gets in right so let’s say Langerhans
23:36
cells gets its most probably longer than
23:38
cells it’s gonna mediate the first time
23:39
because in the skin you get a you can
23:41
have a lot of drunken cells which is the
23:43
skin dendritic cells but this time
23:46
though it doesn’t really need to go to
23:47
the lymph node because a naive T helper
23:50
cell the ninetieth boxing cells have
23:52
already been been presented and now we
23:55
have memory cells of to berkeley and
23:57
these memory cells can either be
23:59
scattered around your skin for example
24:01
or they can be in the in the lymph nodes
24:04
now all this dendritic cells need to do
24:06
is to present birth cling to the own
24:09
image
24:10
to the memory t-cells th one gets
24:14
activated and releases interferon gamma
24:16
that activates macrophages which is
24:19
specialized in inflammation so this one
24:23
is going to release interleukin one like
24:25
in sixth and terminal critical for alpha
24:27
which acts as pro-inflammatory meaning
24:31
they’re going to increase the
24:32
permeability of the blood vessel that
24:34
causes water and also white blood cells
24:37
to to flow in and cause edema which is a
24:41
swelling due to too much fluid in the
24:43
interstitial space another thing that
24:46
could happen is that it could get inside
24:48
the cell or even between the cells and
24:51
that could cause the effector T
24:53
cytotoxic cell to actually kill the cell
24:57
that are infected with the tuberculin so
25:00
I hope this video at least helped you a
25:03
little bit to understand the
25:04
hypersensitivity and I hope this was
25:06
helpful