How can the innate immune system influence autoimmunity in type 1 diabetes and other autoimmune disorders?
The environment is important in determining the onset of autoimmune diseases such as type 1 diabetes. Genetic susceptibility factors interact with the environment to trigger and modulate a series of immune responses that ultimately lead to destruction of the insulin-producing beta cells of the pancreas. Although T lymphocytes are thought to play a major pathogenic role in the pathogenesis of diabetes, undoubtedly other components of the immune system also contribute to this process. How the environment may alter the course of disease is unknown, although viruses have been implicated in triggering and/or exacerbating the disease process. In this review, we will focus on how infection, particularly with viruses, may influence the onset of type 1 diabetes and other autoimmune diseases. Mechanisms such as molecular mimicry, bystander activation, and uncontrolled polyclonal activation of the immune system may contribute to the immune pathogenesis. We will also explore the interaction of the innate immune system with adaptive immune responses in predisposing individuals to the development of autoimmunity.
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Section of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, Mailbox 208020, 333 Cedar Street, New Haven, CT 06520, USA. li.wen@yale.edu
Wong
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D000818:Animals; D001327:Autoimmune Diseases / Q000628:therapy / Q000821:virology*; D015551:Autoimmunity; D003922:Diabetes Mellitus, Type 1 / Q000628:therapy / Q000821:virology*; D004195:Disease Models, Animal; D006801:Humans; D007113:Immunity, Innate; D051379:Mice; D014777:Virus Diseases / Q000276:immunology*