Type II Hypersensitivity – Antibody mediated – 5-8h (Abbas pp 209)

IgE causes Type 1 Hypersensitivity. What about other antibodies? Other antibodies can cause disease by directly binding to antigens in cells and tissues (type II), or by forming antigen-antibody complexes (type III) which deposit in blood vessels. Usually, the antibodies that cause the disease are against self-antigens, and rarely against microbial infections. One example of such a case is: streptococcal infections. Antibodies against these cross react with heart muscle therefore causing rheumatic fever. Sometimes the antibody can deposit in kidney glomeruli causing glomerulonephritis.

Mechanism of tissue injury and disease

• Antigens may deposit in cells or tissues, and antibodies (IgG & IgM) produced against these specific antigens may deposit in cells and tissues as well causing injury by inducing local inflammation or interfering with normal cellular functions.

• Clinical examples of a Type II hypersensitivity reaction are:

  • Foetal problems: Foetus Rh +ve, mother Rh –ve. Mother starts making antibodies against foetus. 1^st pregnancy is fine, but 2^nd pregnancy (if foetus is Rh +ve again) will cause problems due to maternal antibodies attacking foetus.

  • G rave’s Disease: antibodies act as hormones and bind to hormone receptors in the Thyroid gland. Cause increase production of thyroid hormone.

  • Myasthenia gravis: antibodies against Ach receptors at neuromuscular junctions cause inhibition of receptors. Therefore skeletal muscle contraction does not occur ≫ paralysis.

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• IgG & IgM antibodies bind to neutrophil and macrophage Fc receptors activating these cells. This results in inflammation. The same antibodies, this time including IgM, activate the complement system by the classical pathway resulting in production of complement by-products that further recruit leukocytes ≫ inflammation. Leukocytic activation means these cells produce reactive oxygen intermediates and lysosomal enzymes that damage adjacent tissues.

• Another process is by opsonisation. The antibody may fixate on platelets or red cells with antigen, which opsonises these cells therefore increasing the efficiency of phagocytosis.

Category: Pathology Notes