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TGF-β and IL-6 drive the production of IL-17 and IL-10 by T cells and restrain TH-17 cell–mediated pathology

TGF-β and IL-6 drive the production of IL-17 and IL-10 by T cells and restrain TH-17... Studies have shown that transforming growth factor-β (TGF-β) and interleukin 6 (IL-6) are required for the lineage commitment of pathogenic IL-17-producing T helper cells (TH-17 cells). Unexpectedly, here we found that stimulation of myelin-reactive T cells with TGF-β plus IL-6 completely abrogated their pathogenic function despite upregulation of IL-17 production. Cells stimulated with TGF-β plus IL-6 were present in the spleen as well as the central nervous system, but they failed to upregulate the proinflammatory chemokines crucial for central nervous system inflammation. In addition, these cells produced IL-10, which has potent anti-inflammatory activities. In contrast, stimulation with IL-23 promoted expression of IL-17 and proinflammatory chemokines but not IL-10. Hence, TGF-β and IL-6 'drive' initial lineage commitment but also 'restrain' the pathogenic potential of TH-17 cells. Our findings suggest that full acquisition of pathogenic function by effector TH-17 cells is mediated by IL-23 rather than by TGF-β and IL-6. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Immunology Springer Journals

TGF-β and IL-6 drive the production of IL-17 and IL-10 by T cells and restrain TH-17 cell–mediated pathology

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References (55)

Publisher
Springer Journals
Copyright
Copyright © 2007 by Nature Publishing Group
Subject
Biomedicine; Biomedicine, general; Immunology; Infectious Diseases
ISSN
1529-2908
eISSN
1529-2916
DOI
10.1038/ni1539
Publisher site
See Article on Publisher Site

Abstract

Studies have shown that transforming growth factor-β (TGF-β) and interleukin 6 (IL-6) are required for the lineage commitment of pathogenic IL-17-producing T helper cells (TH-17 cells). Unexpectedly, here we found that stimulation of myelin-reactive T cells with TGF-β plus IL-6 completely abrogated their pathogenic function despite upregulation of IL-17 production. Cells stimulated with TGF-β plus IL-6 were present in the spleen as well as the central nervous system, but they failed to upregulate the proinflammatory chemokines crucial for central nervous system inflammation. In addition, these cells produced IL-10, which has potent anti-inflammatory activities. In contrast, stimulation with IL-23 promoted expression of IL-17 and proinflammatory chemokines but not IL-10. Hence, TGF-β and IL-6 'drive' initial lineage commitment but also 'restrain' the pathogenic potential of TH-17 cells. Our findings suggest that full acquisition of pathogenic function by effector TH-17 cells is mediated by IL-23 rather than by TGF-β and IL-6.

Journal

Nature Immunology – Springer Journals

Published: Nov 11, 2007

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