936 Antigen-presenting cells from HCA2-KO mice are defective in activating regulatory T cells

Gut commensal microbes affect the mucosal immune system via expansion of regulatory T cells (Treg) in colon. This is mediated short-chain fatty acids (SCFA), bacterial metabolites generated during fiber fermentation. SCFA are also produced by skin bacteria and may activate resident Treg, activity which diminished certain inflammatory dermatoses. Only upon binding to G-protein coupled receptors, exert their antiinflammatory effects. A relevant receptor for HCA2. Since ligation HCA2 causes suppression intestinal inflammation, we studied whether absence might be responsible recently described impaired Treg HCA2-knock out mice (HCA2-KO). Adoptive transfer experiments isolated from lymph nodes spleens sensitized wild type (WT) HCA2-KO revealed that WT-Treg significantly reduced contact hypersensitivity recipient animals, whereas this effect was not observed recipients HCA2-KO-Treg. To study HCA2-deficiency affects antigen-presenting cells, bone marrow-derived dendritic (BMDC) WT or were examined flow-analysis. BMDC failed release IL-10 aldehyde dehydrogenase 1A involved generation forkhead box P3 (Foxp3) positive Treg. phenotype losing capacity induce prove potency priming coculture performed. CD4+T mixed with presence hapten. removed after 48h flow analysis CD4+ conducted. as potent inducing Foxp3, glycoprotein repetitions predominant, cytotoxic T-lymphocyte-associated protein 4 on co-cultured comparison WT-BMDC. These results suggest deficiency alters DC such a way they any longer able induce/activate