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Immunol Rev. 2008 Dec;226:132-46. doi: 10.1111/j.1600-065X.2008.00714.x.

From interleukin-23 to T-helper 17 cells: human T-helper cell differentiation revisited.

Author information

1
Department of Immunology, Schering-Plough Biopharma (Formerly DNAX Research), Palo Alto, CA 94304, USA.

Abstract

Protracted inflammation leading to dysregulation of effector T-cell responses represents a common feature of a wide range of autoimmune diseases. The interleukin-12 (IL-12)/T-helper 1 (Th1) pathway was thought to be responsible for the pathogenesis of multiple chronic inflammatory diseases, including psoriasis, inflammatory bowel disease, arthritis, or multiple sclerosis, mainly through their production of interferon-gamma and its effects on macrophage activation and chemokine production. However, this initial concept of T-cell-mediated chronic inflammation required an adjustment with the discovery of an IL-12-related cytokine, designated IL-23. IL-23 was rapidly recognized for its involvement in the establishment of chronic inflammation and in the development of a Th cell subset producing IL-17, designated Th17, which is distinct from the previously reported Th1 and Th2 populations. This review aims to describe the characterization of IL-23 and its receptor, its biological activities, as well as its involvement in the development of human Th17 cells and autoimmunity.

PMID:
19161421
PMCID:
PMC3660846
DOI:
10.1111/j.1600-065X.2008.00714.x
[Indexed for MEDLINE]
Free PMC Article

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