Hypersensitivity

Abstract

Hypersensitivity reactions may be defined as tissue damage occurring in close proximity to an immunological reaction which is primarily designed to cause the rejection of foreign antigen from the tissues. Two types of mechanism are involved. The first is referred to as ‘cell-mediated immunity and the reaction is between antigen and “specifically sensitized lymphocytes’. In this process macromolecular pharmacological agents are released which act on macrophages and cause inflammatory reactions of the delayed hypersensitivity type. The second type of hypersensitivity reactions are those known as immediate hypersensitivity. These reactions are mediated by humoral antibodies which are circulating immunoglobulin molecules. Anaphylactic type reactions are caused by IgE molecules and result in the release of vasoactive amines from tissue mast cells. Arthus reactions and tissue lesions are caused by the deposition of ‘immune complexes’ formed between antigen and other types of immunoglobulins which activate the complement system. Immune complexes are deposited in small blood vessels and cause a necrotizing vasculitis. Glomerulonephritis, arthritis, cutaneous vasculitis, myocarditis and iridocyclitis are now recognized as features of ‘immune complex disease’. Circulating immune complexes in the form of mixed cryoglobulins may give a clue as to the nature of the extrinsic antigen causing the disease, as the association of these states with cryoglobulinaemia has been found to occur in certain infectious conditions.