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

By K. Hirota, J. Duarte, M. Veldhoen, E. Hornsby, Y. Li, D. Cua, H. Ahlfors, C. Wilhelm, M. Tolaini, U. Menzel and 3 more. Nature Immunology, 2011

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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 (TH17 cells) had distinct plasticity in different inflammatory settings. Chronic inflammatory conditions in experimental autoimmune encephalomyelitis (EAE) caused a switch to alternative cytokines in TH17 cells, whereas acute cutaneous infection with Candida albicans did not result in the deviation of TH17 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-TH17 cells'). Thus, this model allows the actual functional fate of effector T cells to be related to TH17 developmental origin regardless of IL-17 expression.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/86dad86890cc5259336d94f927268cccd167ed8d

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Citations in the corpus

Development and maintenance of regulatory T cells. (2013, background): “…seen between Th1 and Th17 cells; the distribution pattern of DNaseI-hypersensitive sites within the Ifng locus is similar between activated Th17 and Th1 cells, consistent with the ability of Th17 cells to produce IFN-g under Th1-cell-polarizing conditions (Hirota et al., 2011; Mukasa et al., 2010).”