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Molecular bases of immune complex pathology

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Abstract

The binding of antigens with antibodies forms immune complexes in the body. Usually these complexes are eliminated by the system of mononuclear phagocytes without development of pathological changes. This review highlights principal mechanisms responsible for safe removal of immune complexes in primates and humans. Special attention is given to diseases known as “immune complex diseases”, when antigen-antibody complexes induce inflammatory reactions. The review considers key experimental works that significantly contributed to current knowledge of etiology and pathogenesis of type III hypersensitivity. Some factors of the development of immune complex syndrome such as level of humoral immune response to antigen, isotype and affinity of forming antibodies, the amount of immune complexes, and the consequences of their interaction with the complement system and Fc-receptors are analyzed based on the molecular mechanisms involved. The review contains a retrospective analysis of the most significant scientific achievements in immune complex pathology investigation within the last 100 years.

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Abbreviations

C5aR:

receptor for C5a

CIC:

circulating immune complexes

CR1:

receptor for C3b

DNP:

2,4-dinitrophenol

FcR:

Fc receptor

PAF:

platelet activating factor

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Correspondence to K. V. Shmagel.

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Original Russian Text © K. V. Shmagel, V. A. Chereshnev, 2009, published in Biokhimiya, 2009, Vol. 74, No. 5, pp. 581–592.

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Shmagel, K.V., Chereshnev, V.A. Molecular bases of immune complex pathology. Biochemistry Moscow 74, 469–479 (2009). https://doi.org/10.1134/S0006297909050010

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