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This video is part 2 of Acquired Immunity – Antibodies.
All information in my immunology videos is sourced from:
Antibody Structure:
Introduction
0:00
in this video we’re gonna look at
0:01
antibodies antibodies are plasma
0:04
proteins known as immunoglobulins now to
Where do Antibodies Come From?
0:07
understand the different immunoglobulins
0:09
we have in our body I feel like it’s
0:11
most natural to know where they come
0:13
from first right so we got our b-cells
0:16
right here right chillin in the cortex
0:17
of the lymph node I’ll show you a scheme
0:19
later B cells have was called b-cell
0:21
receptors on the surface composed of
0:23
either IgG or IgM antibodies which are
0:26
membrane bound and a single transducer
0:29
as a heterodimer called IgA and RGB
0:31
those are those transmit the signal to
0:34
the nucleus when the IgG or IgM binds to
0:37
something right so now let’s imagine
0:40
this antigen right here was just catched
0:42
from the interstitial fluid from the
0:44
lymph vessel and then brought to the
0:46
cortex of the lymph node and it was
0:48
unlucky enough to accent the fit to the
0:51
membrane bound antibody on the surface
0:53
of the B cell it’s then gonna perform an
0:55
antigen B cell receptor endocytosis and
0:58
present a fragment of the antigen an MHC
1:02
class 2 molecule remember b-cells are
1:04
also antigen presenting cells – at the
1:07
same time at the rate Excel can also
1:08
phagocyte and the antigen and eventually
1:11
presented an MHC class 2 molecule
1:13
remember generating cells and B cells
1:15
are both professional antigen presenting
1:17
cells because they can’t present
1:19
fragments of peptides to T cells of an
1:22
MHC class 2 module now the dendritic
1:24
cell is going to present the fragment on
1:27
the MHC class molecule to a naive T
1:29
helper cell so the naive T helper cell
1:32
will dock to the MHC class 2 molecule
1:34
with its T cell receptor and this hope
1:37
that works kind of an anchor is called
1:40
cd4
1:41
a cd4 is very good at binding to MHC
1:44
class 2 models then it will send a
1:47
signal to an the nucleus through the CT
1:49
3 molecule this whole thing is what we
1:52
call TCR MHC complex and I haven’t
1:55
really talked about this yet I’ll go
1:56
through it in details when I go through
1:58
the antigen presenting cells but all
2:01
antigen presenting cells Express b7
2:04
which binds to cd28 on the T helper cell
2:08
there’s a very important core receptors
2:10
to signal to the T helper cell to
2:13
we differentiate into either th one or
2:16
th – then after it binds to b7 through
2:19
cd28 it will start expressing
2:22
interlocking for receptors which is also
2:24
very important in differentiating on
2:27
naive T helper cell to T helper cell –
2:30
and the interlocking four is usually
2:32
secreted out by other T helper cells –
2:35
or master cells or basophils or it can
2:38
also actually sometimes be secreted out
2:41
by the naive T helper cell itself which
2:43
can bind to its own interlocking four
2:47
receptor is called an antigen function
2:49
right now after it is received into
2:52
looking for it will then start to to
2:55
secrete out into the king – which will
2:58
bind to its own receptor that’s also
3:01
called an antiquated function the
3:03
interlocking – is gonna help the naive T
3:05
helper cell to grow and proliferate and
3:09
differentiate into an active T helper
3:12
cell – it’s can differentiate into many
3:13
T helper cell – right and then after its
3:17
its differentiates and and proliferate
3:20
it’s gonna help the initial active B
3:23
cell to proliferate remember B cells is
3:26
also an antigen presenting cell if this
3:28
dendritic cells wasn’t there this B cell
3:30
could do exactly the same as what the
3:32
antigen presenting cells did to the
3:34
naive T helper cell right it also
3:36
expresses b7 now after the T helper
3:40
cells get active it expresses something
3:42
called cd4 he likened which will bind to
3:46
cd4 T on the active B cell so when a
3:48
b-cell gives activated after it binds to
3:51
an antigen it starts expressing cd4 t
3:55
cd4 t cd40 ligand those two when they’re
3:58
connected those are very important core
4:00
receptors that help the B cell
4:03
differentiate now what happens T helper
4:06
cell 2 is going to secrete into looking
4:08
for its kinetically interlocking files
4:10
can secrete integral 6 and clerking 10 +
4:13
T helper cell 1 can secrete out
4:15
intellection 2 or interferon gamma each
4:20
one of these are responsible to what
4:23
kind of antibody
4:24
this B cell is going to start to release
4:27
now if we need more immunoglobulins type
4:29
a for example in the mucous membranes T
4:32
helper cell to release will release more
4:35
interlocking v if we need more IgG T
4:38
helper cell – will release more
4:40
interlocking for and even interferon
4:43
gamma from the T helper cell one will
4:45
trigger the IgG production right so it
4:48
doesn’t really receive all of those at
4:50
once now this B cell can start to
4:54
differentiate into a plasma cell which
4:56
secretes immunoglobulins and also it’s
4:59
going to differentiate into a memory B
5:01
cell in case we were to get exposed to
5:04
the same type of antigen the future for
5:06
quicker response those antibodies will
5:09
go bind to the antigen which will
5:11
neutralize them kind of inhibiting them
5:14
if that makes sense
5:16
it will also optimize them make it
5:18
easier for right blood cells that can
5:20
phagocyte bind and then actually engulf
5:23
this antigen and even activate the
5:25
classical pathway of the complement
5:27
system right so that’s how they’re
5:30
produced antibodies look like this right
Components of an Antibody
5:33
what’s the components let’s use its
5:36
diagram to help us make it easier
5:38
I’ll show only one half of the
5:40
immunoglobulin the other half is
5:42
identical right and antibody has a light
5:45
chain that that’s the one in yellow and
5:47
a heavy chain that’s one in green right
5:49
it has a variable portion that’s that’s
5:52
the first two it’s kind of logical when
5:53
you think about it because that’s where
5:55
the antigen is kind of bind so it has to
5:57
be variable because different antibodies
5:59
bind different antigens and has a
6:02
constant region which is constant now we
6:07
can fill a variable plus light chain
6:10
equals VL constant plus LC equals CL
6:14
variable plus heavy chain equals BH
6:18
constant plus heavy chain equals ch1 ch2
6:23
and ch3 right it’s not really at the
6:26
heart if you think about it the CL and
6:29
ch1 is connected through D so feed bonds
6:32
and they’re also pounds here connecting
6:35
the two parts of the antibody and they
6:37
form this hinge
6:38
region the hinge is really important
6:41
because it allows the antibody to bind
6:43
to antigens much efficiently as you see
6:46
right here in this picture so you know
6:49
these two floppy upper parts
6:51
they’re called fab this stands for
6:54
fragment antigen binding and it can bind
6:57
different epitopes in the antigen
6:59
depending on the variable region the
7:02
lower part is FC I call it f constant
7:05
but it really stands for fragment
7:08
crystallizable region for some reason
7:09
the FC region is where macrophages can
7:12
bind and complement system now I will
7:15
try not to confuse you too much here but
7:18
the antibody has domains right the
7:21
variable domain are where the antigen
7:24
binds CH one region that reminds the
7:27
other type I’ll get more into that later
7:30
in this video but a low type is when two
Domains
7:33
of the same type of antibody has
7:36
different CH one region cuz there ll of
7:40
the same constant gene differs but don’t
7:43
worry too much about that right now
7:45
alright CS two domains is where the c1
7:48
of the complement system binds CH three
7:52
domains is where cells with FC receptor
7:55
binds like the macrophages B lymphocytes
7:57
and mast cells for example now this is
8:00
the most important part antibodies have
8:03
different variants of chains right the
8:06
light chain here in yellow can be either
8:08
lambda chain or gun or copper chain
8:10
there really no functional difference
8:12
between them but the heavy chain though
8:15
this is the most important part because
8:17
we’re gonna have five different types of
8:19
immunoglobulins in our body at least
8:21
what we know of gamma me Alpha Delta and
8:25
epsilon chain that stands for IgG IgM
8:28
IgA IgG in IgE now let’s go through each
8:32
and every one of these and see what
8:33
their characteristics are right the IgG
IgG
8:37
or the antibody with gamma chain exists
8:40
only as a monomer I’m not gonna go into
8:42
much detail to this but IgG also have
8:45
subclasses it has a GG one to four now
8:48
if you would analyze your blood you
8:50
would see that around
8:52
25% of the immunoglobulins in your
8:54
plasma are going to be IgG antibodies
8:57
IgG is the only antibody that gives us
9:00
passive immunity from our mother by
9:02
placenta transfer before we were born
9:05
because of that you know the x-axis is
9:07
gonna be the age in mom and the y-axis
9:10
here shown in percent it’s gonna be the
9:13
concentration of immunoglobulins who
9:14
have in our plasma now when were first
9:17
born all the immunoglobulins we have in
9:20
our blood is gonna be IgG and those are
9:22
from our mothers right as you see here
9:25
this decreased slightly towards when we
9:27
reach six months and then they increase
9:30
because we start to develop our own
9:32
adaptive immunity IgG can either help
9:36
with a direct opsonization can help
9:39
phagocytes actually bind to the macro
9:42
organism and they’re also really really
9:44
good at activating the classical pathway
9:46
of the of the complement system
9:48
so that’s idg RJM is a special one it’s
IgM
9:53
mostly found as a pentamer
9:55
bound together by a jade chain as you
9:58
see here you can also find these as a
10:00
monomer bound to the surface of b-cells
10:03
IgM is what we call the youngest class
10:06
because the fetus can actually produce
10:08
those on their own
10:10
and you can see it doesn’t really start
10:12
from zero concentration when you’re born
10:13
cool right it’s most probably because
10:16
IgM can be produced without the help of
10:19
t-cells I’ll get more into that later
10:20
now there’s one thing I have to talk
10:25
about when I mentioned IgM and IgG I’m
10:27
now going to talk too much about it as
10:29
it’s for another topic the fuchsia video
10:32
but you know let’s say this is you right
10:35
when you get infected by the bacteria so
10:38
it’s the first antigen exposed to right
10:40
the IgM is gonna react first that that’s
10:44
called the primary response while the
10:46
second exposure after you’ve recovered
10:49
and around 28 days have passed the same
10:52
reaction happens rgm doesn’t really give
10:54
you any sort of memory since t-cells are
10:57
not involved in production of IgM
11:00
b-cells can just differentiate into IgM
11:03
producing plasma cells when they bind to
11:05
the antigen
11:06
and because there is no t-cells involved
11:08
no memory B cells are produced GG in the
11:12
other hand they will react the same way
11:14
in the primary humoral response and as
11:16
you see it started later because the
11:18
process of getting IgG is a little
11:20
longer because it involves t-cells but
11:22
they will form memory B and T cells for
11:25
a quicker and stronger immune response
11:27
in the secondary humoral immune response
11:30
during the second exposure right what
11:34
else can a GM do it can activate the
11:36
complement system the same way as IgG
11:38
does and they do exist as monomers on
11:42
the surface of B cells remember the B
11:45
cells have BCR receptors which composed
11:47
of either a GM or IG d so that’s our gen
11:52
next our GA our da are found by Mary
IgA
11:55
also with a jade chain and it’s mostly
11:58
found at the portals of entry so this is
12:02
the mucosal epithelium right here on the
12:04
Left there’s alumna propria and the
12:06
lumen to the right so I hope you kind of
12:09
get a sort of an image of what we’re
12:11
looking at right now I’m really bad at
12:12
animating things so in London
12:15
appropriate you can have plasma cells or
12:18
what we call alpha plasma cells because
12:21
these plasma cells are specialized in
12:23
secretion of IgE antibodies and they’re
12:27
gonna bind the epithelium with the help
12:29
of what is called Pooley iga receptors
12:32
and be transported through the cytoplasm
12:35
via endocytosis and then they’re going
12:39
to be secreted out through proteolytic
12:41
cleavage to attack any type of specific
12:43
bacteria or virus they were initially
12:45
produced against now keep in mind that I
12:49
GA is a predominant immunoglobulin in
12:52
the sarah mucus such as the saliva milk
12:55
Tokyo bro health and guinea to renal
12:59
secretion also I’m not gonna go into
13:01
much detail into this but there are two
13:02
subclasses also IG a1 and RJ ita2 but we
13:07
will leave it like that
13:09
one thing though is that many
13:12
microorganisms have adapted to the
13:15
environment in the upper respiratory
13:16
tract early
13:17
seeing proteins that Cleaves IgA those
13:21
sneaky little things you may find them
13:24
as monomeric or trimeric as well in
13:27
terms of concentration IgA represents
13:29
roughly roughly about 15 to 20 percent
13:32
of adult human serum immunoglobulin pool
13:35
because most of them are found in the
13:38
mucus next we have itd we have very low
IgD
13:42
amount of them in the serum under 1% and
13:45
the reason is that most of them are
13:46
found on the surface of B cells or on
13:50
the surface of mature B cells to be
13:51
exact
13:52
they exist therefore mostly as monomeric
13:55
the precise role of IgE DES a little
13:58
unclear yet but they are on the surface
14:01
of B cells so they do help them bind and
14:04
differentiate other studies have found
14:07
that they increase in number of idd
14:09
during our two immune diseases during
14:12
chronic inflammation and also increases
14:16
an amount if there are any sorts of
14:18
tumors that’s really all ahead for a GD
IgE
14:22
I GD rge on the other hand is very low
14:26
amount in the blood as well because they
14:29
exist as monomers found on the surface
14:33
of mast cells and basophils and they
14:36
play a role in type 1 hypersensitivity
14:37
in allergic reactions and the first step
14:41
of obtaining IgE is through
14:43
sensitization since the decision is the
14:46
first step of allergies it’s when let’s
14:49
say breathe in pollen for example for
14:50
the first time and then the poem is
14:52
gonna get into the mucosa because
14:54
epithelium presented to antigen
14:57
presenting cells and then that’s gonna
14:59
cause an immune response producing IgE
15:01
so because of that you will find an
15:04
increase amount in allergic disorders
15:06
and also parasite infections as well so
15:11
that was all the antibodies now there is
15:14
one more thing I wanted to talk about
15:16
there are some differences between the
Differences Between Antibodies
15:19
antibodies we can have idiotypic
15:21
differences where the antibody differs
15:24
in the variable region like the one you
15:27
see right here for example both IgG bind
15:30
to different
15:31
engines we can also have isotopic
15:34
antibodies differ in their constant
15:37
regions and we can have a loti big
15:40
differences remember that one where
15:41
we’re gonna have two of the same IgG but
15:45
they’re gonna have differences between
15:47
them because they have different alleles
15:50
of the same constant genes that cause
15:52
for ch1 so lastly I made this list I
Table to Memorize
15:57
hope it can be a little helpful to you
15:59
we can go through everything together
16:01
right now just quickly IgG right here is
16:05
mainly monomer and it you will find most
16:08
of it in the serum around 70 to 75
16:11
percent and their role is to optimize to
16:14
activate a complement remember and
16:16
remember you receive them passively from
16:19
your mother during fetal life through
16:21
the placenta so a passive immunity in
16:24
newborn right rgm in the other hand you
16:27
can find them as pentameric circulating
16:30
in your blood or monomeric on the
16:32
surface of b-cells around 10% you’ll
16:35
find them in the serum and they can
16:37
activate the complement system and they
16:39
can also bind to antigens surface and
16:42
ops and eyes as well our GT in the other
16:46
hand
16:46
those are exist as monomers it’s logical
16:49
because you are mostly finding them on
16:51
the surface of b-cells but you’ll also
16:53
find some of them in the serum under 1%
16:56
and if they come from b cell development
17:01
and their role is also related to B
17:05
cells as well
17:06
IgA mostly time Eric you can find them
17:10
as trimeric and mullah Mary but they
17:12
exist mostly in them because of lumen
17:14
and also some of them in the serum 15 to
17:18
20 percent their role is to protect you
17:21
from microorganisms by agglutinating the
17:25
microorganism settle at the luminal of
17:27
the mucosal surface right
17:29
lastly IgE exists only as monomeric on
17:33
the surface of mast cells and also
17:35
basophils in the tissues and you can
17:38
also find fragments of them in the
17:41
theorem and
17:42
percent as well and these guys are
17:44
against parasites and they cause
17:46
anaphylactic shock by activating mast
17:48
cells or basa fields into releasing
17:50
their mediators which cause anaphylactic
17:53
shock
17:54
so that was mainly everything I wanted
17:57
to talk about my only tips is that if
17:59
you write down this table several times
18:01
maybe you will then remember the
18:04
antibodies easier
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