T-helper 17 cells articles within Nature

Featured

• Letter | 19 December 2018

  Metabolic heterogeneity underlies reciprocal fates of T_H17 cell stemness and plasticity

  Phenotypically, transcriptionally and metabolically diverse subsets of T_H17 cells develop in a chronic autoimmune disease: one subset has inferred stemness features and low anabolic metabolism, while a reciprocal subset has higher metabolic activity that supports transdifferentiation into T_H1 cells.

  • Peer W. F. Karmaus
  • , Xiang Chen
  •  & Hongbo Chi

• Letter | 25 October 2017

  Reversing SKI–SMAD4-mediated suppression is essential for T_H17 cell differentiation

  TGFβ signalling regulates T helper 17 (TH17) cell differentiation by reversing SKI–SMAD4-mediated suppression of RORγt, revealing a potential therapeutic target for treating TH17-related diseases.

  • Song Zhang
  • , Motoki Takaku
  •  & Yisong Y. Wan

• Letter | 17 July 2011

  Control of T_H17 cells occurs in the small intestine

  • Enric Esplugues
  • , Samuel Huber
  •  & Richard A. Flavell

• News & Views | 27 April 2011

  A helping hand against autoimmunity

  The T_H17 helper cells of the immune system have a dark side: they mediate autoimmune disorders. Two drugs that prevent the differentiation and activity of these cells might be of therapeutic value. See Letters p.486 & p.491

  • Anton M. Jetten

• Letter | 17 April 2011

  Suppression of T_H17 differentiation and autoimmunity by a synthetic ROR ligand

  • Laura A. Solt
  • , Naresh Kumar
  •  & Thomas P. Burris

• Letter | 27 March 2011

  Digoxin and its derivatives suppress T_H17 cell differentiation by antagonizing RORγt activity

  • Jun R. Huh
  • , Monica W. L. Leung
  •  & Dan R. Littman

• Letter | 20 October 2010

  Generation of pathogenic T_H17 cells in the absence of TGF-β signalling

  CD4⁺ T cells that selectively produce interleukin (IL)-17 (T_H17 cells) are essential for host defence and autoimmunity. It has been thought that IL-6 and transforming growth factor (TGF)-β1 are the factors responsible for initiating the specification of T_H17 cells. Here, however, it is shown that T_H17 differentiation can occur in the absence of TGF-β signalling. IL-6, IL-23 and IL-1β effectively induced IL-17 production in naive precursors. These data reveal an alternative mode for T_H17 differentiation and the importance of IL-23.

  • Kamran Ghoreschi
  • , Arian Laurence
  •  & John J. O’Shea

• Letter | 01 April 2010

  IκBζ regulates T_H17 development by cooperating with ROR nuclear receptors

  Interleukin-17-producing helper T (T_H17) cells are a distinct T-cell subset characterized by its role in autoimmune disease. Here it is shown that the development of T_H17 cells requires the transcription factor IκBζ, as well as nuclear receptors of the ROR family. Mice lacking IκBζ have a defect in T_H17 development and are resistant to the induction of experimental autoimmune encephalomyelitis. The study points to some new potential molecular targets for drugs to treat autoimmune disease.

  • Kazuo Okamoto
  • , Yoshiko Iwai
  •  & Hiroshi Takayanagi