IL-10 signaling in dendritic cells controls IL-1β-mediated IFNγ secretion by human CD4⁺ T cells: relevance to inflammatory bowel disease.

ABSTRACT: Uncontrolled interferon γ (IFNγ)-mediated T-cell responses to commensal microbiota are a driver of inflammatory bowel disease (IBD). Interleukin-10 (IL-10) is crucial for controlling these T-cell responses, but the precise mechanism of inhibition remains unclear. A better understanding of how IL-10 exerts its suppressive function may allow identification of individuals with suboptimal IL-10 function among the heterogeneous population of IBD patients. Using cells from patients with an IL10RA deficiency or STAT3 mutations, we demonstrate that IL-10 signaling in monocyte-derived dendritic cells (moDCs), but not T cells, is essential for controlling IFNγ-secreting CD4⁺ T cells. Deficiency in IL-10 signaling dramatically increased IL-1β release by moDCs. IL-1β boosted IFNγ secretion

SUBMITTER: Veenbergen S 

PROVIDER: S-EPMC6752724 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature