Mixed results with modulation of TH-17 cells in human autoimmune diseases.
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.
Steinman
Lawrence
L
Department of Neurological Sciences and Interdepartmental Program in Immunology, Beckman Center for Molecular Medicine, Stanford University School of Medicine, Stanford, California, USA. steinman@stanford.edu
D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D061067:Antibodies, Monoclonal, Humanized; D001327:Autoimmune Diseases / Q000276:immunology* / Q000378:metabolism; D002454:Cell Differentiation / Q000276:immunology*; D006801:Humans; D053762:Interleukin-12 Subunit p40 / Q000276:immunology / Q000378:metabolism; D020381:Interleukin-17 / Q000276:immunology* / Q000378:metabolism; D008954:Models, Biological; D020529:Multiple Sclerosis, Relapsing-Remitting / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology* / Q000378:metabolism; D000069549:Ustekinumab
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D053762:Interleukin-12 Subunit p40; D020381:Interleukin-17; D000069549:Ustekinumab