Research ArticleT CELL DIFFERENTIATION

TH17 cells require ongoing classic IL-6 receptor signaling to retain transcriptional and functional identity

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Science Immunology  17 Jul 2020:
Vol. 5, Issue 49, eaaw2262
DOI: 10.1126/sciimmunol.aaw2262

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TH17 sustenance via IL-6

The pathogenic role of the TH17 subset of CD4+ T cells in multiple immune-mediated diseases has prompted close scrutiny of the cytokine signals that promote differentiation and maintenance of TH17 cells. IL-6 and TGF-β are key cytokines for TH17 commitment by naïve T cells whereas IL-23 supports maintenance of a TH17 identity. Harbour et al. investigated whether persistent IL-6 signaling is also needed to sustain TH17 cell functions. IL-6Rα–deficient mouse T cells could not maintain a TH17 phenotype and were attenuated in their ability to elicit colitis in an in vivo cell transfer model. These studies provide deeper insights into the set of signals required for TH17 cell maintenance and suggest additional molecular targets for pharmacological interventions aimed at antagonizing pathogenic TH17 immunity.

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