期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 42, 期 9, 页码 2263-2273出版社
WILEY
DOI: 10.1002/eji.201242598
关键词
Autoimmunity; Hallmark cytokines; IL-23; Polarization
类别
资金
- EMBO long-term Fellowship [ALTF-508-2011]
- Forschungskredit of the University of Zurich
- Swiss National foundation (SNF)
- Swiss MS Society
During the past decade, it has been firmly established that IL-23 is essential for disease development in several models of autoimmune disease, including psoriatic skin inflammation, inflammatory bowel disease (IBD), and experimental autoimmune encephalomyelitis (EAE). The mechanism by which IL-23 exerts its pathogenic role has been mostly scrutinized in the context of Th17 cells, which were thought to mediate autoimmunity by secretion of IL-17 family cytokines. However, the picture emerging now is one of multiple IL-23-responsive cell types, pro-inflammatory cytokine induction, and pathogenic licensing following an IL-23-dominated interaction between the T cell and the antigen-presenting cell (APC). This review will focus on our changing view of IL-23-dependent autoimmune pathologies with a particular emphasis on the responder cells and their IL-23-induced factors that ultimately mediate tissue destruction.
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