Journal
CLINICAL IMMUNOLOGY
Volume 111, Issue 3, Pages 225-233Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.clim.2004.01.008
Keywords
interferon alpha; type 1 diabetes; autoimmunity
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Funding
- NCRR NIH HHS [M01 RR00051, M01 RR00069] Funding Source: Medline
- NIAID NIH HHS [AI 50864, AI 46374, AI 39213] Funding Source: Medline
- NIDDK NIH HHS [DK 32083, DK 55969, DK 62718, P30 DK57516] Funding Source: Medline
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The incidence of type 1 diabetes has been rapidly rising. Environmental factors such as viruses have been implicated as a possible agent accounting for this rise. Enteroviruses have recently been the focus in many research studies as a potential agent in the pathogenesis of type 1 diabetes. The mechanism of viral infection leading to beta cell destruction not only involves multiple pathways but also the cytokine-interferon alpha (IFN-alpha). Our hypothesis is that activation of toll receptors by double-stranded RNA or poly-IC (viral mimic) through induction of IFN-alpha may activate or accelerate immune-mediated beta cell destruction. Numerous clinical case reports have implicated that IFN-alpha therapy is associated with autoimmune diseases and that elevated serum IFN-alpha levels have been associated with type 1 diabetes. In multiple animal models, given specific genetic susceptibility, poly-IC can induce insulitis or diabetes. Therapeutic agents targeting IFN-a may potentially be beneficial in the prevention of type 1 diabetes and autoimmunity. (C) 2004 Elsevier Inc. All rights reserved.
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