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Autoimmunity: increasing suspects in the CD4+ T cell lineup

Abstract

Chronic reactivity of CD4+ T cells to autoantigens and to components of the commensal flora drive destructive inflammation in a variety of mouse models of autoimmunity. Insight gained using these models is empowering translational research into human disease. Immunologists are trying to assign disease culpability to one of the ever-growing number of T helper (TH) cell subsets. Although recent discovery of the interleukin 17–producing TH-17 lineage appeared to supplant the pre-eminence of TH1 cells in promoting autoimmunity, the newest data defy simple paradigms. Here we speculate on the respective contributions to autoimmunity made by an increasingly complex list of TH subsets and argue that the TH1 phenotype may be staging a comeback.

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Figure 1: Primary polarization of diverse CD4+ T cell subsets.
Figure 2: Chain sharing among the IL-12 family of cytokines, and among their receptors, warrants provisional attributions.

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Acknowledgements

Supported by the US National Institutes of Health (C.T.W. and M.T.P.) and the Crohn's and Colitis Foundation of America (C.T.W. and M.T.P.).

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Correspondence to Matthew T Palmer or Casey T Weaver.

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Palmer, M., Weaver, C. Autoimmunity: increasing suspects in the CD4+ T cell lineup. Nat Immunol 11, 36–40 (2010). https://doi.org/10.1038/ni.1802

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