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Induction of a colitogenic phenotype in Th1-like cells depends on interleukin-23 receptor signaling [in vivo]

ABSTRACT: Th1 cells were adoptively transferred into RAG1 KO mice from either wildtype (Il23rwt/eGFP) or KO (Il23reGFP/eGFP) donors. At the peak of disease in recipients of wildtype cells, the animals were euthanized and intestinal T cells were isolated from the chosen recipients of both wildtype and KO cells for 10x massively parallel single-cell RNA-sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE164519 | GEO | 2021/05/01

REPOSITORIES: GEO

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Induction of a colitogenic phenotype in Th1-like cells depends on interleukin-23 receptor signaling.

Project description:Interleukin-23 receptor plays a critical role in inducing inflammation and autoimmunity. Here, we report that Th1-like cells differentiated in vitro with IL-12 + IL-21 showed similar IL-23R expression to that of pathogenic Th17 cells using eGFP reporter mice. Fate mapping established that these cells did not transition through a Th17 cell state prior to becoming Th1-like cells, and we observed their emergence in vivo in the T cell adoptive transfer colitis model. Using IL-23R-deficient Th1-like cells, we demonstrated that IL-23R was required for the development of a highly colitogenic phenotype. Single-cell RNA sequencing analysis of intestinal T cells identified IL-23R-dependent genes in Th1-like cells that differed from those expressed in Th17 cells. The perturbation of one of these regulators (CD160) in Th1-like cells inhibited the induction of colitis. We thus uncouple IL-23R as a purely Th17 cell-specific factor and implicate IL-23R signaling as a pathogenic driver in Th1-like cells inducing tissue inflammation.

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Induction of a colitogenic phenotype in Th1-like cells depends on interleukin-23 receptor signaling

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Induction of a colitogenic phenotype in Th1-like cells depends on interleukin-23 receptor signaling [cytokine cultures]

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Identification of IL-23 target genes in intestinal CD4+ T cells

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