Induction and protection of autoimmune rheumatic diseases. The role of infections.
It is thought that in genetically predisposed individuals, autoimmune diseases can be promoted and/or exacerbated by viruses, bacteria, or parasitic infectious agents. Pathogens can activate innate immune response interacting with Toll-like receptors that recognize pathogen-associated molecules. As a consequence of infections, a prolonged inflammatory response may occur leading to chronic inflammation with activation of adaptive immune response. In addition, the defective clearance of apoptotic infected cells, which progress- es to secondary necrosis, can foster the autoimmune reactions. Although numerous data from humans and/or animal models support the hypothesis of a direct contribution of pathogens to the induction of the disease, some infectious agents are able to prevent autoimmune disorders. In this review, data on the innate and adaptive immune response induced by pathogens are summarized, focusing on the possible protective or non-protective role of infections in the development of autoimmune diseases.
Department of Pathology, University of Cambridge, Cambridge, UK.
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Cooke
G F
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Ferraccioli
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Herrmann
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Romani
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Schulze
S
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Zampieri
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Doria
D000818:Animals; D001327:Autoimmune Diseases / Q000382:microbiology* / Q000821:virology*; D006801:Humans; D007239:Infections / Q000150:complications* / Q000276:immunology*; D012216:Rheumatic Diseases / Q000276:immunology / Q000382:microbiology / Q000821:virology