Th17 cells express interleukin-10 receptor and are controlled by Foxp3− and Foxp3+ regulatory CD4+ T cells in an interleukin-10 dependent manner
By S. Huber, N. Gagliani, E. Esplugues, William O'Connor, Francis J. Huber, A. Chaudhry, M. Kamanaka, Yasushi Kobayashi, C. Booth, Alexander Y. Rudensky and 3 more. Immunity, 2011
603 citations recorded by the source corpus.
Summary T helper 17 (Th17) cells are important for host defense against extra-cellular microorganisms. However they are also implicated in autoimmune and chronic inflammatory diseases, and as such need to be tightly regulated. The mechanisms that directly control committed pathogenic Th17 cells in vivo remain unclear. We showed here that IL-17A-producing CD4+ T cells expressed interleukin-10 receptor α (IL-10Rα) in vivo. Importantly, T cell specific blockade of IL-10 signaling led to a selective increase of IL-17A+IFN-γ− (Th17), and IL-17A+IFN-γ+ (Th17+Th1) CD4+ T cells during intestinal inflammation in the small intestine. CD4+ Foxp3− IL-10 producing (Tr1) cells and Foxp3+ regulatory (Treg) were able to control Th17 and Th17+Th1 cells in an IL-10-dependent manner in vivo. Lastly, IL-10 treatment of mice with established colitis decreased Th17 and Th17+Th1 cells frequencies via direct signaling in T cells. Thus IL-10 signaling directly suppresses Th17 and Th17+Th1 cells.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/d43b45028cca99ef9ef6c78e948ffa4b8ade391c
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In Immunology
- Alexander Y. Rudensky
- C. Iadecola
- A. Chaudhry
- P. Treuting
- Robert Samstein
- Yuqiong Liang
- Werner Müller
- J. Anrather
Citations in the corpus
- Commensal microbiota affects ischemic stroke outcome by regulating intestinal γδT cells (2016, positive): “Intestinal T reg are indispensable for maintaining an anti-inflammatory environment in the gut by suppressing T H 17 cell differentiation 12,13 and γδ T cell proliferation 14 .”
- Interleukin-10 signaling in regulatory T cells is required for suppression of Th17 cell-mediated inflammation (2011, positive): “Furthermore, impaired IL-10 signaling in effector T cells results in augmented Th17 cell but not Th1 cell responses, and Treg cells can restrain these Th17 cell responses in an IL-10dependent manner (Huber et al., 2011).”
- Molecular aspects of the pathogenesis of periodontitis. (2015, background): “The key cytokine involved in T-helper type 1 differentiation is interleukin-12 (1, 41).”
- Activation of the receptor (Gpr109a) for niacin and the commensal metabolite butyrate suppresses colonic inflammation and carcinogenesis (2014, positive): “IL-10 deficiency leads to spontaneous colitis (Huber et al., 2011; Izcue et al., 2009; Rubtsov et al., 2008).”