期刊
NATURE REVIEWS RHEUMATOLOGY
卷 6, 期 1, 页码 40-49出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nrrheum.2009.237
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- NIDCR NIH HHS [R37 DE012354] Funding Source: Medline
- NATIONAL INSTITUTE OF DENTAL &CRANIOFACIAL RESEARCH [R37DE012354] Funding Source: NIH RePORTER
A significant body of data implicates the type I interferon (IFN) pathway in the pathogenesis of autoimmune rheumatic diseases. In these disorders, a self-reinforcing cycle of IFN production can contribute to immunopathology through multiple mechanisms. Type I IFN cytokines are pleiotropic in their effects, mediating antiviral and antitumor activities, and possess numerous immunomodulatory functions for both the innate and adaptive immune responses. A key principle of the type I IFN system is rapid induction and amplification of the signaling pathway, which generates a feed-forward loop of IFN production, ensuring that a vigorous antiviral immune response is mounted. Although such feed-forward pathways are highly adaptive when it comes to rapid and effective virus eradication, this amplification can be maladaptive in immune responses directed against host tissues. Such feed-forward loops, however, create special opportunities for therapy.
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