IL-23 drives a pathogenic T cell population that induces autoimmune inflammation

Journal of Experimental Medicine - Tập 201 Số 2 - Trang 233-240 - 2005
Claire L. Langrish1, Yi Chen2, Wendy M. Blumenschein3, Jeanine Mattson3, Beth Basham4, J D Sedgwick2, Terrill K. McClanahan3, Robert A. Kastelein2, J. Daniel2
1Discovery Research, DNAX Research Inc., Palo Alto, CA 94304, USA.
21Discovery Research, DNAX Research Inc., Palo Alto, CA 94304
32Experimental Pathology and Pharmacology, DNAX Research Inc., Palo Alto, CA 94304
43Bioinformatics, DNAX Research Inc., Palo Alto, CA 94304

Tóm tắt

Interleukin (IL)-23 is a heterodimeric cytokine composed of a unique p19 subunit, and a common p40 subunit shared with IL-12. IL-12 is important for the development of T helper (Th)1 cells that are essential for host defense and tumor suppression. In contrast, IL-23 does not promote the development of interferon-γ–producing Th1 cells, but is one of the essential factors required for the expansion of a pathogenic CD4+ T cell population, which is characterized by the production of IL-17, IL-17F, IL-6, and tumor necrosis factor. Gene expression analysis of IL-23–driven autoreactive T cells identified a unique expression pattern of proinflammatory cytokines and other novel factors, distinguishing them from IL-12–driven T cells. Using passive transfer studies, we confirm that these IL-23–dependent CD4+ T cells are highly pathogenic and essential for the establishment of organ-specific inflammation associated with central nervous system autoimmunity.

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Journal of Experimental Medicine

Tập 201 Số 2

233-240

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