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 PMID:15657292  

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

Claire L Langrish | Yi Chen | Wendy M Blumenschein | Jeanine Mattson | Beth Basham | Jonathan D Sedgwick | Terrill McClanahan | Robert A Kastelein | Daniel J Cua
The Journal of experimental medicine | 2005

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-gamma-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.

Pubmed ID: 15657292

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C57BL/6J (tool)

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BALB/cAnNCrl (tool)

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laboratory mouse with name BALB/cAnNCrl from MGI.

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