Serum Sickness

Ekaterini Paizis and Brendan F Murphy, Department of Nephrology, St Vincent's Hospital, Victoria, Australia

Serum sickness is a type III hypersensitivity reaction that develops after exposure to xenogeneic proteins. It was first described by Von Piquet and Schick in 1905, who noted the development of rash, fever, lymphadenopathy and athralgia in some recipients of xenogeneic sera - horse serum for diphtheria. The pathogenesis of this serum sickness was attributed to the host's immunological reaction to injected antigens and has been described as a generalized Arthus reaction.

Serum sickness was proclaimed as an important experimental model of human immunological disease. In the 1950s several elegant animal studies using radiolabeled serum proteins conclusively demonstrated the association of the pathological lesions of serum sickness with the detection of circulating immune complexes. Circulating and tissue-bound immune complexes form at the time of immune elimination: for a number of factors determine whether circulating immune complexes are deposited in tissues rather than cleared by the reticuloendothelial system. These factors include vascular permeability, local hemodynamic flow, size of complexes and affinity of the antibody. Once deposition takes place, there is activation of the complement cascade and release of chemotactic factors with resultant leukocyte infiltration which results in a characteristic inflammatory response in the target organ.

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