Intestinal resident CX3CR1+ cells support gut immune system by helping production of IgA from B cells

Abstract

Abstract Intestinal resident CX3CR1+ cells are known to sample neighboring or circulatory antigens and present them to CD8+ T cells via cross-presentation. Here we show that intestinal CX3CR1+ cells co-cultured with B cells can induce production of IgA. Unlike intestinal CD103+ DCs, CX3CR1+ cells are independent of retinoic acid and signals from commensal microbiota to induce production of IgA. CX3CR1+ cells express BAFF, APRIL and TNF-α which is required for IgA class-switching of B cells. Intravenous injection of soluble OVA in mice can promote production of IgG and IgA in the serum and feces. Intestinal CD103+ DCs are known to present to CD4+ T cells, however CX3CR1+cells present antigens to CD8+ T cells via cross-presentation. Addition of OT-I cells further enhances production of IgA of B cells co-cultured with CX3CR1+cells. Intestinal CX3CR1+cells are tissue resident cells and do not migrate to the MLN. CCR7 deficiency or FTY720 treatment does not affect the production of intestinal IgA after intravenous injection of OVA in mice. These results suggested that intestinal CX3CR1+cells have an important role in maintaining homeostasis of the intestinal immune system.