Fate mapping of interleukin-17 producing T cells in inflammatory responses

Brigitta B Stockinger (1) , Keiji Hirota (1) , Joao H Duarte (1) , Marc Veldhoen (1) , Eve Hornsby (1) , Ying Li (1) , Daniel J Cua (1) , Mauro Tolaini (1) , Ursula Menzel (1) , Anna Garefalaki (1) , Alexandre J Potocnik (1) , Christoph Wilhelm (1) , Helena Ahlfors (1)

1 Division of Molecular Immunology

We describe a reporter mouse strain designed to fate-map cells that have activated IL-17A. Here we show that TH17 cells show distinct plasticity in different inflammatory settings. Chronic inflammatory conditions in EAE caused a switch to alternative cytokines in TH17 cells, whereas acute cutaneous infection with Candida albicans, did not result in deviation of TH17 to alternative cytokine production, although IL-17A production was shut off in the course of the infection . During development of EAE, IFN-γ and other pro-inflammatory cytokines in the spinal cord were produced almost exclusively by 'ex-TH17' cells whose conversion was driven by IL-23. Thus, this model allows relating the actual functional fate of effector T cells to TH17 developmental origin irrespective of IL-17 expression.

Mots clés: T cells; Inflammation; Pathogenesis

Brigitta B Stockinger, Keiji Hirota, Joao H Duarte, Marc Veldhoen, Eve Hornsby, et al.. Fate mapping of interleukin-17 producing T cells in inflammatory responses. Nature Immunology, 2011, ⟨10.1038/ni.1993⟩. ⟨hal-00612703⟩