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Chapter: Pharmaceutical Microbiology : Immunology

Hypersensitivity can be defined as an exaggerated response of the immune system leading to host tissue damage.



Hypersensitivity can be defined as an exaggerated response of the immune system leading to host tissue damage. However, some of the immune responses described in the hypersensitivity classification below are, in some circumstances, appropriate responses to invading antigen. For example, a component in what is an appropriate immune response to tissue transplant rejection can be defined as a type II hypersensitivity reaction.

The highly influential Gell and Coombs classification scheme defines four categories of hypersensitivity:

•        Type I—immediate hypersensitivity

This is also called anaphylactic or acute hypersensitivity. It involves IgE antibody and is mediated via degranulation of mast cells leading to release of preformed factors which promote an influx of immune cells to the site of mast cell activation and initiation of a rapid inflammatory reaction. In the extreme case the inflammatory response extends beyond the localized site of initiation and affects systemic tissues leading to life-threatening anaphylactic reactions such as those documented to penicillin, to peanut antigen, or to bee-sting antigen. Examples of localized type I hypersensitivity include hay fever. The term ‘allergy’ has become synonymous with type I hypersensitivity.

•        Type II hypersensitivity—antibody-mediated cytotoxicity

This is caused by antibodies that are directed against cell surface antigens. IgG and IgM are the key antibodies involved that direct cytotoxic events against the cell surface with which they interact. The cytotoxic events include activation of the classical complement pathway leading to the formation of a MAC, and the attraction and activation of killing cells such as NK cells or phagocytes which can bind to the antigen–antibody complex via receptors for antibody Fc domains or complement C3b. Type II hypersensitivity disorders include blood transfusion reactions arising from mismatch of the blood ABO antigens between donor and recipient, or haemolytic disease of the newborn. Autoimmune disorders such as myasthenia gravis, Goodpasture’s syndrome and autoimmune haemolytic anaemias are initiated by autoantibodies reacting against ‘self ’ tissue.

•        Type III hypersensitivity—complex-mediated

This involves the formation of large antigen–antibody complexes that circulate in the blood, are usually coated by complement proteins and are removed by phagocytosis. If this process is compromised for any reason then the antigen–antibody complexes will be deposited in tissue capillary beds, with kidney deposition being clinically the most important site. This deposition of high molecular weight antigen–antibody complexes in the glomerular capillaries of the kidney can lead to a condition termed glomerulonephritis which involves disruption of the glomerular basement membrane, destruction of glomeruli and ultimately renal failure which may necessitate organ transplantation. Systemic lupus erythematosus is a condition where autoantibodies are directed against the host’s DNA and RNA with subsequent complement coated immune complexes deposited throughout systemic tissues such as in the kidney, skin, joints and brain.

•        Type IV hypersensitivity—cell-mediated

This results from inappropriate accumulation of macrophages at a localized site, and may or may not involve the presence of antigen. Under conditions of ongoing localized infection or inflammation, macrophages release proteases, which destroy infected or otherwise damaged tissue. However, with the inappropriate recruitment and/or activation of excessive numbers of macrophages, continuing damage to normal tissue may result, leading to chronic inflammation. The recruitment and activation of macrophages in type IV hypersensitivity is augmented by the activity of helper T-lymphocytes (specifically the TH1 subpopulation). Examples of type IV hypersensitivity include granuloma formation and contact dermatitis. Granulomas are initiated and maintained by the recruitment of macrophages into the site of a persistent source of antigen or toxic material. A granuloma is a fibrotic core of tissue composed of tissue cells and macrophages surrounded by lymphocytes and then further surrounded by layers of calcified collagenous material. Sarcoidosis is a granulomatous disease of unknown cause but characterized by granuloma nodule formation in the lung and skin, among other sites.

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