Transcript ABO blood groups and the immune system

Immune System
Part II
B cells have surface
receptors also but
the receptors are
IgM and IgD. One
B cells may have
10,000 of the AB.
Each one of the AB
are pre programmed
to recognize and bind to specific AG. There is a huge diversity of B
cells due to their variable region. Until activated, these are virgin B
cells.
Vast array of virgin B cells and virgin T cells- very few like one
another are waiting to go into action in secondary lymphoid tissue.
Specific Immune response has two parts
I.Cell mediated response-Involves T-cells killing infected cells
II.Humoral response-Involves Helper T-cells and B-cells which
produce AB to eliminate pathogens.
This process is called clonal selection works because it involves the
specific selection of AG specific T cells and B cells. Virgin B and T
cells will be called into action by the primary immune response in a
process called clonal selection- It is call the clonal selection because
it involves the rapid selection of single lines or clones selected from
vast lymphocyte armies-
Acquired or Specific Immune response has two
parts Cell Mediated and Humoral responses
I. Cell mediated response
1. Macrophages (have both MHC I and MCH
II proteins)
2. Macrophage goes to the site of infection as
part of the nonspecific or innate response
3. The macrophage devours virus, AG, or
bacteria and the macrophage. Bits and pieces of
invader now combine with MHCI and MHCII
proteins. These MHC proteins and AG now are
moved to the plasma membrane. The macrophage (or an infected
cell) is called and antigen presenting cell APC.
Infected cells will also combine bits and pieces of the pathogen with
MHC I proteins and become an APC cell.
4.The macrophage is now
APC .
5. Now the APC
(macrophage) goes to the
virgin T cells looking for
a match between the
TCR (T cell receptor)
receptor and the MCH
protein and antigen on
the APC (macrophage).
When the APC binds
with virgin T-cell a
substance called
interleukin(IL1). IL1 is
a cytokine. Interleukin
(IL1) causes T-cells to
reproduce making
either cytotoxic T-cells,
T-memory cells, or
helper T-cells
depending whether the
match is with a MHC I
and MHCII protein. In
this diagram, it is with
MHC I proteins and
cytotoxic T cells and
memory cells are made.
Meanwhile if a MHC II
protein and antigen makes a
match with a TCR on a T
cell, then the T cell becomes a
helper T cell. In this diagram
the match is with a MCH II
protein. More on helper T
cells later on.
Notes about CD proteins-The
proteins holding the two cells
together are called cluster
differentiation proteins (CD).
CD proteins are found on
lymphocytes. There is a
variety of CD proteins and
different lymphocytes will
contain different CD
proteins. Some
CD proteins are used for adhesion and other CD proteins are used
for as receptors to initiate cell signaling. This is magnified diagram
shows the role of CD proteins on helper T (CD4) and cytotoxic (CD8)
cells. Their function is for adhesion.
While this is
happening, pathogens
are infecting body cells.
Bits and pieces of the
pathogens are inserted
into the MHC I
protein. Either by the
intracellular MHC or
surface MHC. This is
identified as one that is
infected.
While this is
happening, pathogens
are infecting body cells.
Bits and pieces of the
pathogens are inserted
into the MHC I
protein. Either by the
intracellular MHC or
surface MHC. This is
identified as one that is
infected.
The perforin forms pores on the infected
cell. Granzymes cause the cell to undergo
apoptosis and death of the cell. The
cytotoxic cell can go on it merry way to get
rid of other infected cells.
*Cytotoxic cells also kill cancer cells
because cancer cells change and have new
proteins. Some of these new proteins
combine with MHC I proteins and appear
on the surface of the cancer cell. Cytotoxic
cells will combine with cancer cell and kill
it. Every once in a while the cells will
escape the cytotoxic-T-cell because the
MHCI protein has also changed *There is
no longer a dual match and cells replicate or
metastasize
This is another’s rendition of how a cytotoxic cell kills in infected
cell. Below is a cytotoxic cell (orange) killing a cancer cell (purple)
II. Humoral Response involves the arousal of B
cells and antibody formation. Activated
helper-T- cells act much like the macrophages
did in activating virgin T cells.
1. Virgin B cells has AB on surface. It
captures free floating AG which is taken into
the cell.
2. The AG combines with a MCH II protein
and is taken to the surface of the plasma
membrane.
3. Helper-T-cell with its MCH II recognition
site and antigen recognition site finds B-cell
with AG and MHCII protein.
4. The two join and the helper-T-cell
secretes interleukin 2 (IL2) which is a
cytokine. This causes the B-cell to
reproduce.
5. The B-cells fall into 2 types
a. Memory-B-cells for the
secondary immune response
b. Plasma cells which will
produce copious amounts of
AG specific AB
•Any given humoral response
stimulates a variety of different
B cells, each giving rise to a
clone of thousands of plasma
cells.
•Each plasma cell is estimated to secrete about 2,000 antibody
molecules per second over the cell’s 4-5- day life span.
REMEMBER WHAT ANTIBODIES CAN DO!!!!!!!!!!!!!!!!!!!!!!!!!!
They are AG specific.
-AB can bind to several AG
-AB can trigger complement holes in the cell
-Opsonization
Another
drawing of B
cell selection
and
activation of
plasma cells.
Suppressor-T-cells- helps to stop the immune
response
1. Do not know how they are activatedpossibly down AG
2. Thought to stop any further virgin B or T
cells from being activated. So *immune
response stops because plasma cells and
cytotoxic cells only have a short life.
Secondary immune response
Memory cells live for many years If AG comes back the memory
cells( B and T) immediately recognize it. They divide quickly and
get rid of invasion.
The graph shows that it may take two weeks from the initial
exposure to when plasma cells are producing the greatest amount
of antibodies but upon second exposure it only take two days to
produce the same number of antibodies that the initial exposure
caused. In only seven days the number of antibodies in the blood
stream is 100 times the amount produced by the primary response.
This is because of memory cells B cell and memory helper-T cells
Vaccines- used of killed or inactivated viruses that no longer causes
the disease but provides AG which will cause the immune response
making memory cells so that when exposed to the pathogen, there
is a quick secondary immune response
Natural active immunity- (mumps) Exposed to the actual
pathogen and caused the disease. Memory cells were made.
Subsequent exposure to the disease does not cause the disease.
Artificial active immunity- (vaccine) Given inactive parts of the
pathogen so that memory cells were made. Subsequent exposure
to the disease does not cause the disease.
Natural passive immunity- AB in breast milk and the IgG
antibodies of a pregnant woman cross the placenta to her fetus.
Lasts a few weeks to a few months
Artificial passive immunity- shot with AB in the antiserum from
an animal that has already had the disease. Passive immunity can
be transferred artificially by injecting antibodies from an animal
that is already immune to a disease into another animal. For
example, a person bitten by a rabid animal is injected with
antibodies against rabies virus because rabies may progress
rapidly, and the response to an active immunization could take too
long to save the life of the victim.
Lymphocyte diversity and B cellsThere are not enough genes to provide for the diversity of millions of
lymphocytes.
There are app. 300 DNA segments during development the 300
segments are rearranged to produce # different proteins for variable
region of AC (18 billion).
Also AB can be modified once made
T cells- less is known but think may be similar to B cells.
Next slide is an example of how genes are rearranged to form
different AB. The slide after that shows how clonal selection works
in the immune system.
ABO blood groups and the immune system
On the surface of red blood cells there are polysaccharide chains attached
to proteins. The immune system considers them as antigens unless the
person contains that gene. A person with type A blood contains A
antigen whereas a person with type B blood contains B antigen. A
person with type AB blood has both A and B antigens and a person with
type O blood has neither. During the process of lymphocyte maturation,
lymphocytes recognize self and will not make antibodies against the
antigens on its own red blood cells. For example, if one has type A
blood, then one would not make antibodies against the A antigen but
would make antibodies against the B antigen.
There are bacteria in the environment that has proteins similar to the A
and B antigens. When these bacteria enters a person’s body, the body
will make antibodies for any A or B antigen that is not found on one’s
own blood type. Now the person has circulating “ preformed” antibodies
for blood types that the person does not possess. For example a person
with type A blood will have type B antibodies even though
ABO blood groups and the immune system
a person with type A blood will have type B antibodies even though they
have not been exposed to type B blood. This makes blood typing
important in transfusions. The antibody for these antigens are IgM and
do not cross the placenta.
The Rh antigen is another antigen found on red blood cells. There are
several variations of this antigen. It is a protein. If one has it, then they
are Rh+ and if one does not then they are Rh-. There is a problem for a
pregnant women who is Rh- and if her fetus is Rh+. During the first
pregnancy, when birthing the child, some of the baby’s blood will mix
with the mother’s. She will make AB against the Rh antigen. Now the
second pregnancy, if any the blood mixes, her Rh antibodies will cross
the placenta and agglutinate the babies red blood cells called
erythroblastosis fetalis. To prevent this, the mother is injected with antiRh antibodies. This will eliminate any fetal blood cells that should cross
into her body and prevent her from making AB against the Rh factor.
AIDS-Acquired immunodeficiency
syndrome Is caused by a RNA virus.
The virus attaches to CD4 protein
and gains entry into the helper T cell.
(macrophages and brain cells also
have CD4 proteins) Once inside, the
RNA is reverse-transcribed into
DNA. This piece of DNA integrates
itself into the genome of the helper
T -cell. Now it can direct the production of more viruses. The helper T
cell dies because of the damaging effects of the virus. The destruction of
the helper T cell effects both the humoral response and the cell mediated
response. Usually people with AIDS die of secondary infections from
opportunistic pathogens like a pneumonia caused by a fungi or Kaposi’s
sarcoma, a rare cancer. There is no cure for AIDS only a combination of
drugs that slows down the progress of the disease.
A T-cell
being
infected
by the aids
virus (blue
particles)