Description

This video is about Antigen Presenting Cells (APCs).

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

What Are Antigen Presenting Cells (APCs)?

• Phagocytose microorganisms and present them on MHC I or MHC II.
• Express B7 (Co-stimulatory molecule for T-cell activation).
• Present MHC II to naïve T-Helper Cells (CD4+).
• Require three activation signals to activate naïve T-helper cells:
  1. 1st Activation Signal: MHCII-TCR (CD4 and CD3)
  2. 2nd Activation Signal: B7 – CD28
  3. 3rd Activation Signal: Interleukins
• MHC I activates T-cytotoxic cells (CD8+).

Professional Antigen Presenting Cells:

• B-Lymphocytes
• Macrophages
• Dendritic Cells

Inactive/Unprofessional Antigen Presenting Cells:

• Langerhans Cells

B-Lymphocytes:

• Produce antibodies against specific antigens.
• During development: B-cells randomly generate surface antibodies.
• If B-cells do not encounter antigens within a certain timeframe, they undergo apoptosis (Anergy).

B-Lymphocyte Development:

Occurs in the Spongy Bone:

1. Starts as Pluripotent Hematopoietic Stem Cell.
2. Pro B-Cell
3. Pre B-Cell (Heavy chain recombination for IgM: VDJ gene)
4. Immature B-Cell (Light chain recombination: VJ gene, IgM development complete)
5. Mature B-Cell: Expresses both IgM and IgD on the surface.
6. Checked for self-reactivity. If non-self-reactive → Travels to secondary lymphoid organs (Lymph nodes, spleen, Peyer’s patches).

B-Lymphocyte Activation:

• B-Cell Receptor (BCR): Consists of IgD/IgM and signaling chains (Igα and Igβ).
• B-Cells reside in the outer cortex of lymph nodes.

Steps:

1. BCR binds to antigen.
2. Endocytosis of BCR-antigen complex.
3. Antigen is presented on MHC II to Th2 or Th0.
4. Th2 binds to the activated B-cell through:
   • CD40L-CD40 interaction
   • TCR-MHCII interaction
5. Cytokines (IL-4, IL-5, IL-10, IL-6, IL-2, IFN-γ) help B-cell differentiate.
6. B-Cell becomes a Memory B-cell or Plasma Cell.

T-cell Dependent B-cell Differentiation: Produces IgA, IgE, or IgG.

T-cell Independent B-cell Differentiation: Rapidly produces IgM when polysaccharides bind to BCR (No memory B-cells produced).

Macrophage Development:

1. Pluripotent Hematopoietic Stem Cell
2. Mono Stem Cell
3. Pro-monoblast
4. Monoblast
5. Pro-monocyte
6. Monocyte in blood
7. Monocyte differentiates into:
   • Free Macrophage (in tissue)
   • Fixed Macrophage
   • Dendritic Cell

Macrophage Functions:

• MHC I and MHC II expression.
• Fc receptors:
  • Fc IgG (Direct Opsonization)
  • Fc IgE
• C3b receptor: Binds complement protein C3b.
• CD14: Recognizes Lipopolysaccharides (LPS).
• B7: Co-stimulation for T-cell activation.

Active Macrophage Releases:

• Interleukin 12 (IL-12): Differentiates Th0 into Th1 and activates Natural Killer (NK) cells.
• Interleukin 8 (IL-8): Chemotaxis.
• Interleukin 1 (IL-1), IL-6, TNF-α: Act as endogenic pyrogens (cause fever).
• IL-1, IL-6, TNF-α travel to the hypothalamus → Release Prostaglandin E2 (PGE2).
• IL-6 travels to the liver → Causes the release of acute phase proteins.

Dendritic Cells:

• Derived from monocytes in the blood.
• Highly migratory.

Surface Markers:

• MHC I and MHC II
• B7
• Adhesion molecules: Help bind T-lymphocytes.

Langerhans Cells:

• Also known as immature dendritic cells.
• After phagocytosis, they migrate to lymph nodes and begin expressing B7.

Transcript

Introduction
0:00
hello and welcome to another video in
0:01
this video I’m gonna talk about the
0:03
different antigen presenting cells we
0:05
have in our body basically how they
0:07
develop and their characteristics so
Function of Antigen-Presenting Cells (APCs)
0:10
what is an antigen presenting cell these
0:12
cells are cells that can catch
0:15
microorganism and basically present them
0:17
on either MHC 1 or MHC 2 but these guys
0:21
were special with these guys is that
0:23
they can actually Express what is called
0:24
b7 and b7 is a major call simulator for
0:28
the T cells we have in our body so let’s
0:30
put this to practice for example let’s
0:32
say this antigen presenting cell just
0:34
catching or microorganism it then
0:37
migrated to the lymph node through the
0:39
lymph vessels right because the Olympus
0:41
cells drains the interstitial fluid we
0:43
have in the tissue so these guys can
0:46
actually go through them and reach the
0:47
lymph nodes and then reach the naive
0:50
t-cells in they in the power cord as
0:51
I’ll show you later so now it goes to
0:54
the lymph node it presents the peptide
0:56
on the MHC class 2 molecule we can take
0:59
that one first and macey class 2
1:01
molecules can only bind to naive T
1:04
helper cell because naive T helper cell
1:06
is what we call also cd4 cells cd4 is
1:10
what actually docks to the MHC class 2
1:13
as you see right here they’re very good
1:16
at anchoring the cell to towards the MHC
1:18
class 2 so that they can bind and when
1:21
that bind that they actually stimulate
1:23
cd3 as you see right here CD 3 then
1:27
sends a positive signal towards the cell
1:28
three signals are required to activate
1:32
and differentiate the cell the first
1:34
signal is the T cell receptor MHC
1:37
complex the second signal is really
1:39
important as the b7 and cd28 one day by
1:42
together does the second signal now the
1:44
third thing I was going to be cytokines
1:46
and the naive T helper cells going to
1:49
differentiate into different T helper
1:51
cells depending on what kind of
1:53
intelligence they receive so let’s say
1:55
they receive interlocking 12:4
1:57
interferon gamma it’s gonna become T
1:59
helper cell one that’s gonna be mostly
2:02
for inflammation like activated
2:04
macrophages for example or other T sized
2:06
toxic cells if it receives interacting
2:09
for mainly it’s going to differentiate
2:10
into T helper cell to which may
2:12
activates B B lymphocytes or it risk if
2:16
it receives interleukin 6 for example or
2:18
interact in 21 it’s gonna become t
2:20
helper cells 17 which is very
2:22
specialized in parasitic infection for
2:24
example right now
2:27
it can also activate for example T
2:29
cytotoxic cells because this cells are
2:32
very specific in binding MHC class 1 by
2:34
their cd8 again they will activate
2:37
seeded 3 send a positive signal 30
2:39
cytotoxic cell to nucleus of it that’s
2:41
the first signal the second signal is b7
2:43
to cd28 the third thing was usually
2:47
going to be intelligence from T helper
2:50
cell one which helps it to further
2:51
differentiate into effector T so Texas
2:54
cell and differentiate so this was just
2:56
a quick overview of what antigen
2:58
presenting cells mainly do alright so
Types of APC
3:01
the type of antigen presenting cells we
3:04
got B lymphocytes macrophages are also
3:07
very important type of antigen
3:09
presenting cells and we got dendritic
3:11
cells dendritic cells of they are very
3:12
good at co-stimulation because they’re
3:14
very big and they have these processes
3:17
the the dendrites that can actually
3:19
stretch and activate several cells at
3:22
the same time a subtype of dendritic
3:25
cell is the Langerhans cells in the skin
3:27
I will get more into that soon but these
3:30
3 are the main dice these 3 are the real
3:33
antigen presenting cells we call them or
3:34
a better name professional antigen
3:36
presenting cell they’re professional
3:39
because they express MHC and b7 as I
3:42
said earlier both are needed to activate
3:44
and differentiate T cells the reason why
3:47
I put Langerhans cells here is because
3:49
it doesn’t really express b7 Elise walks
3:53
around in the skin that means it’s not
3:55
really a professional antigen presenting
3:57
cell even though it’s a subtype of
3:59
dendritic cell but once it phagocytes it
4:03
catches antigen and it becomes active it
4:06
migrates to lymph node and then Express
4:08
sb7 so once logged on cells goes to a
4:11
lymph node and expresses b7 that’s when
4:14
it becomes an active or a professional
4:16
antigen presenting cell so that’s why I
4:17
had to put the other side to keep in
4:19
mind that not all dendritic cells are
4:21
professional antigen presenting cells
4:24
all the time
4:24
all right so now let’s see where they
4:26
come from and how they function we’ll
B-Lymphocyte Development
4:29
start with the B lymphocytes right so
4:32
you know normally in our body antibodies
4:36
are only produced when we’ve been
4:38
infected with a microorganism and then
4:40
antibodies that are produced will
4:43
normally be specific for that specific
4:45
marker organism right B lymphocytes
4:48
however also Express antibodies on its
4:51
surface it can be either b IG d or r GM
4:54
if it’s not sure right so these two
4:57
antibodies are membrane bound we call
5:00
the membrane bound antibodies their
5:02
primary development happens completely
5:04
without exposure to antigen and that’s
5:07
very weird because we just said that
5:09
antibodies are produced once you have
5:12
been exposed to antigens but B cells
5:15
undergo a lot of gene rearrangement of
5:17
these membrane bound antibodies do you
5:20
have but if they’re not exposed to any
5:22
type of antigen later within a few weeks
5:25
normally they die by apoptosis – to free
5:28
up space for other B cells with their
5:31
rearranged antibodies so the whole
5:33
process is actually random what kind of
5:35
antibodies can bind and the more you get
5:38
exposed to the same type of antigen the
5:41
more rearrangement you will have and the
5:43
more specific is going to be for that
5:46
specific type of antigen all right so
5:48
now let’s see how this works and where
5:51
they come from you know the bone is
5:53
composed of the diocese’s metal faces
5:55
and the epiphysis right so this is a
5:57
femur and inside there are yellow bone
6:00
marrow with a lot of fat cells and
6:03
spongy bone with the red bone marrow
6:05
which is highly vascularized with blood
6:08
vessels and here is where most of the
6:10
red blood cells and Lucas has come from
6:12
including our balloon facade and they
6:15
start off as a pluripotent hematopoietic
6:18
stem cell and then later become probe B
6:22
cell nothing extra really happens here
6:25
other than a few receptor start to
6:27
Express now keep in mind I’m not going
6:29
to go in too much detail into this I’m
6:31
just gonna go through the most important
6:33
part kind of give you a sense of how
6:35
these were
6:36
right so now a probl is then going to
6:39
become a pre B cell here recombination
6:42
of the heavy chain gene or the vdj dean
6:46
happen schematically it looks like this
6:48
with a vdj gene and a constant gene I
6:53
remember an antibody consists of a heavy
6:55
chain and the light chain right now once
6:59
these genes are rearranged and our name
7:02
starts to be produced and heavy chain
7:04
are made now just to be more specific
7:06
new heavy chains are made keep that in
7:09
mind that it only expresses IgM at early
7:13
stage of development right so what we’re
7:16
trying to make now is IgM so membrane
7:18
bound IgM vdj it stands for variable
7:22
diversity and joining in case you were
7:25
wondering now it becomes an immature B
7:28
cell and that’s the final stage before
7:30
it becomes a mature B cell where
7:33
recombination of the light chain gene
7:35
occurs it looks somehow like this with G
7:39
and J genes and there you get recombined
7:42
and we get Kappa or lambda light chain
7:44
which goes with the previous heavy
7:47
chains that we made after the
7:49
recombining in the pre B cell and then
7:51
this is finally going to be a membrane
7:53
bound IgM all right and this is really
7:56
important that an immature B cell only
7:58
expresses memory about IgM but once it
8:01
becomes mature it’s going to have a GM
8:05
membrane bound antibodies and IgD member
8:08
of mat antibodies right so all of this
8:11
happens in the bone marrow and that’s
8:13
why it’s called a b-cell be sent for
8:15
bone marrow so so it develops here T
8:18
cells however T cell first timeless so
8:20
they are made in the bone marrow and
8:22
then they travel to the thymus to
8:24
continue its development
8:26
so b-cell develops in the bone marrow T
8:28
develops in the thymus and now just keep
8:32
in mind that there are a few control
8:33
points here and there and if it lacks
8:35
for example IG parts throughout the
8:38
stages it undergoes apoptosis but if
8:41
everything is cool so far we need to see
8:44
if this immature B cell can actually
8:46
react our own tissue or not
8:48
so if it does react to our own tissue
8:52
it usually undergoes some rearrangement
8:54
to try to fix it but if it really can’t
8:58
if it’s still a reacts our own tissue it
9:01
undergoes apoptosis because we really
9:03
don’t want antibodies coming against our
9:05
own tissues but if it’s non-self
9:07
reactive however it travels to the
9:10
secondary lymphoid organs we have in our
9:12
body which is you know susp laying in
9:14
lymph nodes and some peyer’s patches in
9:16
the intestines for example and then
9:18
become mature B lymphocyte which now
9:21
expresses ID
9:22
rgd and IgM so a mature b-cell
9:25
circulates between the lymph blood and
9:28
secondary lymphoid tissue that is where
9:30
you’re going to find these mature B
9:32
lymphocytes so now let’s continue
B-Lymphocyte Function
9:34
further and see how it undergoes
9:36
differentiation and activation so now we
9:39
got our naive mature B cell with a
9:41
b-cell receptor complex which is
9:43
normally composed of either itd or IgM
9:46
membrane bound antibodies and the signal
9:50
chains
9:50
IG alpha and IG beta so these two
9:53
together the single chains and the
9:55
antibody forms the b-cell receptor so
9:59
let’s say it randomly binds to the
10:02
antigen remember most of these guys are
10:05
in the lymph nodes right and the lymph
10:07
node looks sort of like this it has an
10:10
afferent and efferent lymph vessel and
10:12
you got the medulla here and the power
10:14
cortex where most of the T cells are
10:15
this is called a t-cell zone and then
10:17
we’re gonna have an outer cortex where
10:19
the B cells are this is the B’s alone so
10:23
those naive cells are mostly in the
10:25
primary follicle the cortex and once
10:28
they are activated after they have
10:29
endocytosed the whole PCR receptor with
10:32
the antigen and then presented it on an
10:34
MHC class 2 molecule it traveled to a
10:37
secondary follicle where it gets really
10:39
close or it might even sometimes get
10:41
into the power cortex to ask t-cells for
10:44
help with with differentiation now
10:47
remember b-cells doesn’t phagocyte right
10:50
they pull the PCR receptor and antigen
10:53
complex into the cytoplasm to kill it
10:55
and this process is called PCR mediated
10:58
endocytosis and then present it on
11:01
Seaquest to you what is he here where it
11:03
binds to t-helper cell to the had
11:06
earlier being differentiated from a th
11:09
zero by some other antigen-presenting
11:10
cell or if it meets at t at zero first
11:15
before it meets a th to remember b cells
11:18
are also professional antigen presenting
11:20
cells and they also expressed b7 so if
11:23
it first meets naive T helper cell it
11:27
can induce the whole activation method
11:29
just like any other antigen presenting
11:31
cell and then further differentiate into
11:34
a T helper cell type to to again help it
11:37
differentiate right so in order for the
11:39
T helper cell to to actually bind the
11:41
MHC class 2 molecule it has to already
11:44
recognize that specific type of antigen
11:46
now remember this is still happening in
11:50
the lymph node right activated th to
11:53
express cd4 KL and activate be activated
11:57
b7 Express cd4 T that is also a very
12:00
important Co stimulator to actually help
12:03
this piece of differentiate the last
12:05
important factor for the B cell to
12:08
actually start differentiating it’s
12:09
receiving different kind of intelligence
12:12
it can receive interlocking for from the
12:15
tears to cell can receive Internet in
12:17
five interleukin 6 or into even
12:19
intellect in 10 or it can receive
12:21
introduction to an interferon gamma from
12:23
a T helper cell one now each of these
12:26
cytokines are responsible for what kind
12:29
of antibody this B cell is going to
12:31
start to release if we need for example
12:34
more IG type a in the mucous membranes T
12:37
helper cell to release more interlocking
12:40
v and if we need more IgG for example T
12:43
helper cell two will release more into
12:45
looking for or even interferon gamma
12:47
from th one and which will trigger IgG
12:50
production so it doesn’t really receive
12:52
all of those at once keep that in mind
12:54
alright now the B cell is going to start
12:57
to a differentiate into a plasma cell
12:59
which secretes antibodies and the type
13:03
of antibodies again is all depend on
13:04
what kind of an for kind of side current
13:06
receives and it’s also going to the
13:10
into a memory cell because if we get
13:13
infected with the same type of
13:15
microorganisms in the future we’re gonna
13:17
be able to actually get rid of it even
13:20
faster because we have already memory
13:22
cells of that specific microorganism now
13:26
remember one plasma cell can only
13:28
secrete out one type of immunoglobulin
13:31
can’t just secrete out IgM and IgG and
13:35
IgA at the same time all right so if for
13:38
example it secretes out G antigens we
13:41
call this gum plasma cell or if it
13:44
secretes out IgE we call it a an epsilon
13:48
plasma cell now here is another thing
13:51
that’s also very very important that
13:53
these antibodies the plasma cell
13:55
released after the T helper cell has
13:57
helped the B cell differentiate they’re
14:01
either going to be a ga IgE or IgG not
14:06
IG d because IgD is only on b-cell
14:09
receptor during its development and IgM
14:12
has another mechanism of secretion and
14:17
that because in mechanism of secreting
14:19
IgM type motile is what we call T
14:23
independent B cell differentiation so
14:26
when you first infected with a
14:27
microorganism the first antibody that is
14:32
going to react is the IgM type antibody
14:36
and the reason is is that if you want to
14:39
include T helper cell to help the B cell
14:41
it’s a long process and takes a little
14:43
time but if you want a GM it’s a very
14:47
short process because all we need is an
14:49
antigen binding to a b cell which is
14:51
then going to induce a very strong
14:53
signal inside cell and then trigger it
14:56
to to divide this called the clonal
14:59
expansion and then become an and a
15:01
plasma cell which secretes up GM we call
15:04
this mu type
15:06
plasma cell so usually in order to get i
15:11
GM type antibodies it has to be an
15:14
antigen that contains a lot of
15:16
carbohydrates for example Lipa
15:18
polysaccharides of gram-negative
15:19
bacteria those are very good at
15:22
triggering the cell into differentiating
15:24
into a new type plasma cells secreting
15:27
IgM usually that’s our first response
15:29
but then if you later on meets up with a
15:32
T helper cell you think can get
15:34
triggered into releasing another type of
15:36
plasma cell and also a memory bezel but
15:39
that’s only after it’s it has met Teja
15:42
Brazell so that was everything I had for
Macrophage/Dendritic Cell Development
15:46
the B lymphocytes next let’s look at
15:48
macrophages macrophages also come from
15:51
the bone marrow as what we call
15:52
pluripotent hematopoietic stem cell
15:54
again it’s gonna become a mono stem cell
15:57
then a pro munna blast to become a
16:01
mother blast and then to become a pro
16:03
munal site so let’s just take that one
16:05
again so pure potent tamer to predict
16:08
stem cell right it becomes a ma new stem
16:12
cell so after perfect and table to play
16:14
stem cell because ma new stem cell and
16:16
then pro mono blast and then mono blast
16:19
loses the word pro and after a mono
16:22
blast is become a pro mundo side and
16:24
what’s the next one can you guess if
16:26
problem uno glass becomes mu new blast
16:28
then pro muna site is going to become
16:31
what we call a monocyte which is going
16:34
to circulate in the blood so after pro
16:36
monocyte goes over to the bloodstream it
16:40
becomes monocytes so now that monocyte
16:43
can become several different types of
16:45
phagocytes it can either migrate to the
16:48
tissues and become either a free
16:50
macrophage or fixed macrophage and these
16:53
guys are everywhere you can even find
16:55
them entering the lymph vessels into the
16:57
lymph node what’s interesting though is
17:00
that this blood monocyte can also give
17:03
rise to a dendritic cell so dendritic
17:06
cells and macrophages does have a very
17:08
common at development pathway alright
Macrophage Function
17:13
let’s now look at it
17:15
the functions of the macrophage by
17:17
looking at what they have in the surface
17:19
now it does have a lot of surface
17:23
receptors I just included the most
17:25
important ones right it’s gonna have an
17:27
MHC one logically enough because it’s a
17:29
nucleated cell remember three alpha
17:32
chains alpha 1 alpha 2 and alpha 3 and
17:34
then a constant P 2 it’s gonna have an
17:37
MHC 2 because it is logical because it’s
17:39
an antigen presenting cell it’s gonna
17:41
have alpha 1 alpha 2 and beta 1 beta 2
17:43
it has surface receptors for IgG or the
17:48
FC region of the IgG which helps with
17:51
direct of sensation
17:52
it also has surface receptors for FC IgE
17:56
IgE antibodies are released in a huge
17:59
amount during inflammation for example
18:01
due to allergies this is important
18:04
because macrophages are very related to
18:08
inflammation I’ll show you why in a
18:11
second also it has c3b receptors for
18:14
when the complement system optimizes a
18:16
microorganism this is also really really
18:19
important it has cd14 for the aleppo
18:23
polysaccharides you know the
18:24
gram-negative has lipopolysaccharides on
18:27
their surface of their membrane the
18:28
macrophages are really good at actually
18:30
detecting that and they also have
18:33
mannose receptors for example for the
18:35
sugar molecule manuals which is mostly
18:37
found on capsules of the bacteria for
18:39
example though and the fungi and it has
18:42
b7 of course because it’s a professional
18:44
antigen present so now you know when a
18:48
macrophage phagocytes a microorganism as
18:51
you see right here it’s going to present
18:54
parts of that microorganism on an MHC
18:57
right let’s say this is a mercy class –
19:00
and it’s going to express b7 it’s going
19:03
to bind with a naive T helper cell now
19:05
remember there are 3 activation signals
19:07
for T cells there have the T cell
19:10
receptor and the MHC complex you have
19:12
the b7 and cd28 and the third signal a
19:15
macrophage can release interlocking 12
19:18
which is going to sit on the surface of
19:21
the naive T helper cell and help it
19:23
differentiate into T helper cell 1 and
19:26
why do you want that because
19:27
t-helper cell one can help other
19:29
macrophages activate and also T helper
19:32
cell one can activate T cell toxic cell
19:35
so T helper so one is very related to
19:37
inflammation the same as macrophage and
19:39
that’s why I can activate just really
19:41
want T helper cells zero to become T
19:43
helper cell one because if macrophage is
19:46
activated it’s most probably an
19:48
inflammation or a major infection
19:50
happening I’m not going to much details
19:52
in the T cells right now I’m also gonna
19:54
focus on macrophages right so it can
19:57
release interlocking twelve to get a th
19:58
one keep that in mind but T interlocking
20:01
12 has also another function
20:03
interlocking 12 can activate those big
20:06
guys right here the natural killer cell
20:08
those are also really really good at
20:11
cytotoxicity they’re a part of the
20:13
innate immune system and I’ll talk more
20:15
about that when I talk about the
20:16
cytotoxic immune response now just to
20:20
give you the complete picture it’s not
20:22
really related to macrophages but t-80
20:24
can also receive interning for and
20:27
become T helper cell to right and after
20:30
it receives these it’s going to release
20:31
interacting to to sit on its own
20:33
receptors it’s an adjutant function and
20:35
then it can start to grow and
20:37
proliferate so what else can this
20:39
macrophage release it can release
20:41
interlocking aids and interleukin 8 is
20:44
Ashima taxes for other leukocytes and
20:47
remember chemotaxis has the word taxi in
20:49
it so chemotaxis means that it attracts
20:52
other leukocytes to the area so now as
20:54
this macrophage gets activated by
20:56
binding its receptors to the
20:58
microorganism we agree that it releases
21:00
into a can aid in plugging 12 right it’s
21:03
also going to release interlocking one
21:05
in Logan six and tyranny chronic
21:07
factor-alpha these are called
21:10
pro-inflammatory cytokines which has an
21:13
important function interlocking one can
21:15
activate T lymphocytes and other
21:17
macrophages interleukin 6 activates T
21:20
and B lymphocytes and tumor necrosis
21:23
factor-alpha activates endothelium so
21:25
that the endothelium can start expressed
21:27
receptors for circulating white blood
21:30
cells can attach to and that way it’s
21:32
easier for the white blood cells to
21:34
enter the interstitial space and help
21:37
out
21:38
apart from these three functions all
21:40
three are what we call antigenic
21:43
pyrogens that means that they promote
21:46
fever how you know the hypothalamus the
21:50
hypothalamus actually works like a
21:51
thermostat temperature is ultimately
21:54
regulated in the hypothalamus and these
21:56
three can actually go to the
21:58
hypothalamus and cause it to release
22:01
will called prostaglandin e2 and now
22:03
what happens peripheral vasoconstriction
22:06
happens to reduce the heat loss through
22:08
the skin and a cast the person to feel
22:11
cold but at the same time being very
22:13
warm inside so first a bloody knee –
22:16
triggers are pyrogen it or triggers a
22:19
fever other things is you know the liver
22:23
interleukin 6 can trigger the liver into
22:25
releasing acute phase proteins like
22:27
mannose binding lectin or c-reactive
22:30
protein CRP so the macrophages really
22:33
does play a crucial role in systemic
22:36
response to microorganisms so that was
22:39
these now lastly let’s look at dendritic
Dendritic Cell Function
22:42
cells these cells are my favorite
22:45
they’re they’re really really cool and
22:47
you can find them chilling in the spleen
22:48
or the lymph nodes where the T cells are
22:50
and what they can do is you know in the
22:53
peripheral tissue they can phagocyte any
22:56
type of antigen and present them on an
22:58
MHC class 2 or 1 with a b7 also remember
23:02
and then it can travel to these
23:05
secondary lymphoid organs the lymph node
23:07
for example to present the antigen so
23:09
these cells are experts in presenting
23:12
antigens because they can migrate very
23:15
easily so what’s on their surface you
23:18
get MHC ones logical MHC 2 is also
23:20
logical and b7 right those are very very
23:23
important because all antigen presenting
23:25
cells has to have these plus it has a
23:29
lot of adhesion molecules that promotes
23:31
T lymphocytes attachments they do have
23:35
many other receptors that allows it to
23:37
also bind to microorganisms keep that in
23:39
mind then the same thing happens antigen
23:43
presentation and again pay attention
23:45
here b7 is what makes these cells
23:48
professional antigen presenting
23:51
but lankan hotel doesn’t have that
23:53
doesn’t have b7 so it’s sometimes also
23:57
is referred to as an immature dendritic
23:59
cell they do have ever also Express
24:02
manuals receptors so any type of damage
24:05
or infection in the skin the Langerhans
24:09
cells can react and phagocyte and
24:11
Express a peptide of the marker organism
24:14
on an MHC class 2 molecule and then it
24:17
travels to the lymph node and then it
24:20
can express b7 and become mature
24:23
dendritic cell so that was mainly
24:26
everything I had for antigen presenting
24:28
cells and I hope there’s a double