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Cited by 371

The DOI matches its Crossref record; 58 of the 58 references it cites were found in a registry or an index.

The type I IFN induction pathway constrains Th17-mediated autoimmune inflammation in mice

Open access
Guo, Beichu, Chang, Elmer Y., Cheng, Genhong·2008·Journal of Clinical Investigation

Abstract

IFN-beta, a type I IFN, is widely used for the treatment of MS. However, the mechanisms behind its therapeutic efficacy are not well understood. Using a murine model of MS, EAE, we demonstrate that the Th17-mediated development of autoimmune disease is constrained by Toll-IL-1 receptor domain-containing adaptor inducing IFN-beta-dependent (TRIF-dependent) type I IFN production and its downstream signaling pathway. Mice with defects in TRIF or type I IFN receptor (IFNAR) developed more severe EAE. Notably, these mice exhibited marked CNS inflammation, as manifested by increased IL-17 production. In addition, IFNAR-dependent signaling events were essential for negatively regulating Th17 development. Finally, IFN-beta-mediated IL-27 production by innate immune cells was critical for the immunoregulatory role of IFN-beta in the CNS autoimmune disease. Together, our findings not only may provide a molecular mechanism for the clinical benefits of IFN-beta in MS but also demonstrate a regulatory role for type I IFN induction and its downstream signaling pathways in limiting Th17 development and autoimmune inflammation.

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Metadata

Authors
Guo, B., Chang, E. Y., & Cheng, G.
Venue
Journal of Clinical Investigation
Published
2008-05-01
Volume
118
Issue
5
Pages
1680-1690
ISSN
0021-9738 (ISSN-L)
OpenAlex
W2151109138
Cited by
371
References
58
FWCI
25.70
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: The type I IFN induction pathway constrains Th17-mediated autoimmune inflammation in mice. https://app.cochat.ai/papers/10.1172/jci33342
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Guo, B., Chang, E. Y., & Cheng, G. (2008). The type I IFN induction pathway constrains Th17-mediated autoimmune inflammation in mice. Journal of Clinical Investigation. https://doi.org/10.1172/jci33342

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