Type II hypersensitivity


Type II hypersensitivity, in the Gell and Coombs classification of allergic reactions, is an antibody mediated process in which IgG and IgM antibodies are directed against antigens on cells or extracellular material. This subsequently leads to cell lysis, tissue damage or loss of function through mechanisms such as
  1. complement activation via the classical complement pathway
  2. antibody dependent cell-mediated cytotoxicity or
  3. anti-receptor activity.
The activation of the complement system results in opsonization, the agglutination of red blood cells, cell lysis, and cell death.
These reactions usually take between 2 and 24 hours to develop.

Examples

An example of complement dependent type II hypersensitivity is an acute haemolytic transfusion reaction following transfusion of ABO incompatible blood. Preformed antibody against donor red cell antigens not found in an individual of a particular blood group, bind to the donor red cell surface and lead to rapid complement mediated haemolysis and potentially life-threatening clinical consequences.
Another example of a complement dependent type II hypersensitivity reaction is Goodpasture's syndrome, where the basement membrane in the lung and kidney is attacked by one's own antibodies in a complement mediated fashion.
An example of anti-receptor type II hypersensitivity is observed in Graves disease, in which anti-thyroid stimulating hormone receptor antibodies lead to increased production of thyroxine.
However, there are questions as to the relevance of the Gell and Coombs classification of allergic reactions in modern-day understanding of allergy and it has limited utility in clinical practice.