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The gastric lamina propria of mice that have been experimentally infected with the pathobiont  Helicobacter pylori  hosts a dense network of myeloid cells that includes BATF3-dependent CD103 +  dendritic cells (DCs). We show here that CD103 +  DCs are strictly required for gastric Th1 responses to  H .  pylori  and for  H .  pylori  infection control. A similar dependence of type 1 immunity on CD103 +  DCs is observed in a  Mycobacterium bovis  BCG infection model, and in a syngeneic colon cancer model. Strikingly, we find that not only the expansion and/or recruitment of Th1 cells, but also of peripherally induced, neuropilin-negative regulatory T-cells to sites of infection requires BATF3-dependent DCs. A shared feature of the examined models is the strongly reduced production of the chemokines and CXCR3 ligands CXCL9, 10 and 11 in BATF3-deficient mice. The results implicate BATF3-dependent DCs in the recruitment of CXCR3 +  effector and regulatory T-cells to target tissues and in their local expansion.

BATF3-dependent dendritic cells drive both effector and regulatory T-cell responses in bacterially infected tissues