RelB Deficiency in Dendritic Cells Protects from Autoimmune Inflammation Due to Spontaneous Accumulation of Tissue T Regulatory Cells.

ABSTRACT: Foxp3⁺ regulatory T cells are well-known immune suppressor cells in various settings. In this study, we provide evidence that knockout of the relB gene in dendritic cells (DCs) of C57BL/6 mice results in a spontaneous and systemic accumulation of Foxp3⁺ T regulatory T cells (Tregs) partially at the expense of microbiota-reactive Tregs. Deletion of nfkb2 does not fully recapitulate this phenotype, indicating that alternative NF-κB activation via the RelB/p52 complex is not solely responsible for Treg accumulation. Deletion of RelB in DCs further results in an impaired oral tolerance induction and a marked type 2 immune bias among accumulated Foxp3⁺ Tregs reminiscent of a tissue Treg signature. Tissue Tregs were fully functional, expanded indepe

SUBMITTER: Andreas N 

PROVIDER: S-EPMC6826119 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature