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_H17 cells) had distinct plasticity in different inflammatory settings. Chronic inflammatory conditions in experimental autoimmune encephalomyelitis (EAE) caused a switch to alternative cytokines in T_H17 cells, whereas acute cutaneous infection with Candida albicans did not result in the deviation of T_H17 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_H17 cells'). Thus, this model allows the actual functional fate of effector T cells to be related to T_H17 developmental origin regardless of IL-17 expression. [ABSTRACT FROM AUTHOR]