Abstract

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.

Keywords

BiologyImmunologyProinflammatory cytokineInflammationAutoimmunityInterleukin 23PopulationTumor necrosis factor alphaT helper cellT cellInterleukin 12CytokineCell biologyImmune systemInterleukin 17Cytotoxic T cellMedicineGenetics

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Publication Info

Year
2005
Type
article
Volume
201
Issue
2
Pages
233-240
Citations
3991
Access
Closed

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Claire L. Langrish, Yi Chen, Wendy M. Blumenschein et al. (2005). IL-23 drives a pathogenic T cell population that induces autoimmune inflammation. The Journal of Experimental Medicine , 201 (2) , 233-240. https://doi.org/10.1084/jem.20041257

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DOI
10.1084/jem.20041257