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Fate mapping of IL-17-producing T cells in inflammatory responses.

Here we describe a reporter mouse strain designed to map the fate of cells that have activated interleukin 17A (IL-17A). We found that IL-17-producing helper T cells (T(H)17 cells) had distinct plasticity in different inflammatory settings. Chronic inflammatory conditions in experimental autoimmune encephalomyelitis (EAE) caused a switch to alternative cytokines in T(H)17 cells, whereas acute cutaneous infection with Candida albicans did not result in the deviation of T(H)17 cells to the production of alternative cytokines, although IL-17A production was shut off in the course of the infection. During the development of EAE, interferon-γ (IFN-γ) and other proinflammatory cytokines in the spinal cord were produced almost exclusively by cells that had produced IL-17 before their conversion by IL-23 ('ex-T(H)17 cells'). Thus, this model allows the actual functional fate of effector T cells to be related to T(H)17 developmental origin regardless of IL-17 expression.

Pubmed ID: 21278737


  • Hirota K
  • Duarte JH
  • Veldhoen M
  • Hornsby E
  • Li Y
  • Cua DJ
  • Ahlfors H
  • Wilhelm C
  • Tolaini M
  • Menzel U
  • Garefalaki A
  • Potocnik AJ
  • Stockinger B


Nature immunology

Publication Data

March 15, 2011

Associated Grants

  • Agency: European Research Council, Id: 232782
  • Agency: Medical Research Council, Id: MC_U117512792
  • Agency: Medical Research Council, Id: MC_U117565359
  • Agency: Medical Research Council, Id: U.1175.02.003.00003(60535)
  • Agency: Medical Research Council, Id: U117512792
  • Agency: Medical Research Council, Id: U117563359

Mesh Terms

  • Animals
  • Encephalomyelitis, Autoimmune, Experimental
  • Flow Cytometry
  • Genes, Reporter
  • Inflammation
  • Interferon-gamma
  • Interleukin-17
  • Mice
  • Mice, Knockout
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction
  • T-Lymphocytes