Type II hypersensitivity and it’s mechanism

Type II hypersensitivity reactions is also an autoimmune disease involve antibody-mediated destruction of cells by immunoglobulins of heavy chain classes other than Ig-E. The reaction occurred by binding of Ig-G or Ig-M antibodies to the antigen expressed on the surface of the host cells, which are then destroyed by complement or cell-mediated mechanism. It is also known as Ab-dependent (cytotoxic) hypersensitivity.

Mentioned disorders: Autoimmune haemolytic anaemia, Thrombocytopenia, Erythroblastosis fetalis etc.

Mediators: This reaction is mediated by IgG or IgM antibodies and also some complement proteins.

Description or mechanism of reaction: The reaction of type II hypersensitivity is initiated by the binding of Ig-G or Ig-M antibodies to the antigen present on the surface of the target cells or actually host cells that is perceived by the immune system as foreign. It is leading to the destruction of these host cells.

There are three distinct mechanism of this reaction of type II hypersensitivity.

Firstly, the immunoglobulins (Ig-G or Ig-M) can activate the complement system and can create pores in the membrane of the foreign cells by the formation of membrane attack complex (MAC). It causes lysis of the target cell.

Secondly, the antibodies can mediate cell destruction by another type of cell- mediated destructive process called antibody dependent cell-mediated cytotoxicity (ADCC). In this process the cytotoxic cells, bearing Fc receptors binds to the Fc region of the antibodies present on the surface of the target cell and causes death to the cell.

Finally, the antibody bound to the foreign cells, can act as an opsonin and attract the phagocytic cells. The phagocytic cells contain the Fc receptors or C3b (a complement protein also serves as opsonin) receptor to bind to the antibody-coated target cells. Then phagocytosis occurs and destroy the infected target cells.

Testing of type II hypersensitivity includes both the direct and indirect coombs test.

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