Transforming growth factor-β protein inversely regulates in vivo differentiation of interleukin-17 (IL-17)-producing CD4+ and CD8+ T cells.

Dwivedi VP, Tousif S, Bhattacharya D, Prasad DV, Van Kaer L, Das J, Das G
J Biol Chem. 2012 287 (5): 2943-7

PMID: 22170065 · PMCID: PMC3270951 · DOI:10.1074/jbc.C111.327627

TGF-β is a pleiotropic cytokine that predominantly exerts inhibitory functions in the immune system. Unexpectedly, the in vitro differentiation of both Th17 and Tc17 cells requires TGF-β. However, animals that are impaired in TGF-β signaling (TGF-βRIIDN mice) display multiorgan autoimmune disorders. Here we show that CD4(+) T cells from TGF-βRIIDN mice are resistant to Th17 cell differentiation and, paradoxically, that CD8(+) T cells from these animals spontaneously acquire an IL-17-producing phenotype. Neutralization of IL-17 or depletion of CD8(+) T cells dramatically inhibited inflammation in TGF-βRIIDN mice. Therefore, the absence of TGF-β triggers spontaneous differentiation of IL-17-producing CD8(+) T cells, suggesting that the in vivo and in vitro conditions that promote the differentiation of IL-17-producing CD8(+) T cells are distinct.

MeSH Terms (9)

Animals CD8-Positive T-Lymphocytes Cell Differentiation Lymphocyte Depletion Mice Mice, Knockout Receptors, Transforming Growth Factor beta Th17 Cells Transforming Growth Factor beta

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