2. Blood transfusion and Rh incompatibility are due to Antigen-Antibody interactions.
In both of these case Antigens are found on cell surfaces i.e., RBCs. Antibodies involved in these
reactions are of IgG and IgM classes. These are the examples of Type II Hypersensitivity
reactions.
These are also called Antibody Mediated Reactions that cause host tissue damage when
antibodies directly bind to the antigens on cell surfaces and result in the cellular destruction.
Main Features:
These reactions are triggered by Antigens present on cell surfaces that could be Self-antigen that
is, host’s own cell surface molecules. The antigen could be Modified or Altered Self-Antigen for
example in some people Penicillin bind to the host cell surface molecules that leads to formation
of new epitope. The antigen could be Alloantigen too. These are non-self antigens from
members of same species Eg: ABO and Rh blood group antigens.
3. the cells on which antigens are present could be fixed or free. Fixed could be part of a solid
tissue. Free cells include blood cells such as RBCs or Leukocytes.
As we know, Antibodies involved are targeted against antigens on cell surfaces. These
Antibodies belong to IgG and IgM class. Further, these antibodies may be autoantibodies that
are produced due to failure in self-tolerance mechanisms. They can be alloantibodies too.
Produced during Rh incompatibility.
Other players of immune system that participate in the reaction are: Macrophage, Neutrophil,
Eosinophil, Natural killer cells and Complement proteins.
Examples: Hemolytic Anemia, Blood transfusion reactions, Rh incompatibility, Certain platelet
disorders and Tissue Transplantation rejections(Hyperacute Rejection).
4. Type II Hypersensitivity is also called Antibody-mediated cytotoxic Hypersensitivity.
Mechanism:
1)Complement Activation
2)Opsonization or Opsonized phagocytosis. And
3)Antibody-Dependent Cell mediated Cytotoxicity (ADCC)
Complement Activation:
Complement system consists of a set of proteins in blood plasma that through a cascade of
enzymatic reaction results in the destruction of the target cells.
Suppose, antigens on the RBCs are recognized by the antibodies present in the individual and
are bounded. Now, the complementary C1 protein binds to the Fc regions of the RBC bound
antibodies thus activating the classical complement pathway. Now the destruction of RBC can
happed in 2 ways : by 1)opsonization or opsonized phagocytosis – C3b deposited on the cell
surface acts as opsonins that are coating the cell.
5. Phagocytes such as macrophages have C3b receptors. This leads to the phagocytosis of C3b
coated RBCs. In addition to C3b molecules, antibodies can also act as opsonins as macrophages
and neutrophils also have Fc Receptors.
2nd fate could be 2)Cell lysis by MAC complex: Membrane attack Complex is a pore formed on
the cell surface by C5 to C9 complementary proteins that leads to lysis of the cell.
suppose the antigens are on the cells of a solid tissue (fixed) and the individual had preformed
antibodies that recognize the antigens on the cell surface. Once the antibodies bind to the
antigens, the complement activation is activated. Cell destruction also occurs by Membrane
Attack Cytotoxic Complex. In the complement pathway C3a and C5a are also released. These
proteins result in inflammation along with acting as chemokines and chemoattractants. As a
result, leukocytes such as monocytes, Eosinophils, NK cells and Neutrophils migrate form blood
vessels/circulation to the site of injury.
Here phagocytosis is not possible so, the macrophages release cytotoxic contents onto the
target cells.
6. This causes tissue damage.
Another way the cell destruction can be by Antibody-Dependent Cell-mediated
Cytotoxicity(ADCC): this is defined as the process of killing antibody coated target cells by
certain leucocytes such as natural killer cells having specific Fc receptors for these bound
antibodies.
This results in direct lysis of antibody coated cells.
These mechanism result due to cases such as Hyperacute Graft Rejection(HAR), which refers
to the destruction of graft immediately after transplantation. This occurs due to the pree-
existing antibodies present in the recipient’s circulation. These antibodies recognize the
alloantigens present on the endothelial cells of blood vessels within the graft such as ABO
antigens and MHC1 antigens.
7. It is problematic when the donor organ is highly vascularized such as kidney.
Graft is destroyed due to complemented mediated endothelial damage, inflammation,
intravascular thrombosis and hemorrhage of blood into graft.
