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Mixed results with modulation of TH-17 cells in human autoimmune diseases

Nature Immunology volume 11, pages 41–44 (2010)Cite this article

Abstract

The outcomes of clinical trials provide the most convincing data to clarify the role of particular cytokines in the pathogenesis of human diseases. The immunology community, for a variety of practical reasons, spends most of its research time and funds on studies in model systems, mainly mice. In this perspective I discuss results of clinical trials assessing the effect of blocking the differentiation and/or function of interleukin-17–producing CD4+ T cells on human autoimmune disease, and devote more limited attention to corroborating preclinical studies from animal models. Thus far, these outcomes in human trials have been mixed, with notable success in psoriasis and Crohn's disease but a negative result in relapsing-remitting multiple sclerosis.

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Figure 1: IL-12 p40–specific monoclonal antibodies target both IL-12 (a heterodimer of p40 and p35) and IL-23 (a heterodimer of p40 and p19).

Katie Vicari

Figure 2: Cytokines promoting the differentiation and effector function of TH1 and TH-17 cells in humans.

Katie Vicari

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  1. Department of Neurological Sciences and Interdepartmental Program in Immunology, Beckman Center for Molecular Medicine, Stanford University School of Medicine, Stanford, California, USA

    Lawrence Steinman

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Correspondence to Lawrence Steinman.

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Steinman, L. Mixed results with modulation of TH-17 cells in human autoimmune diseases. Nat Immunol 11, 41–44 (2010). https://doi.org/10.1038/ni.1803

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