Vitamin A is a central modulator of bacteria and immune crosstalk in the intestine. (A) SFB produce RA and promote defense against intestinal infection through epithelial RA signaling (63). (B) SFB induce expression of a retinol binding protein, SAA. Retinol is mobilized from epithelium by binding to SAAs and delivered to myeloid cells through LRP1-mediated endocytosis. Myeloid cells may also acquire retinol and/or retinoic acid by unknown pathways. RA produced by myeloid cells is a central regulator of immune homeostasis by regulating differentiation and intestinal homing of T and B cells (23). (C) Commensal bacteria regulate RA pathways in multiple ways. Bifidobacterium infantis increases RALDH expression by DCs to promote anti-inflammatory responses. Clostridia species and Faecalibaculum suppress epithelial RA synthesis, which then reduces IL-22-dependent antimicrobial responses (64) and promotes epithelial turnover through IEL production of IFN-γ (65). (D) Epithelial RA signaling increases IL-18 production and induce cell shedding and IFN-γ production, which promotes the clearance of pathogen (71).