Abstract
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.
Highlights
Arnold & Zhang et al report that CD103+ dendritic cells (DCs) are required for protective Th1 responses, infection control of mucosal and systemic bacterial pathogens, and antitumor immunity driven by CD4+ Th1 cells and CD8+ T cells
Having observed that CD103+ DCs are recruited to the H. pylori-infected gastric mucosa [12], we examined their functional contribution to H. pylori-specific immunity in mice that lack the transcription factor basic leucine zipper transcription factor ATF-like 3 (BATF3)
To rule out that possible differences in the microbiota composition of WT and BATF3-/- mice drive the observed differences in H. pylori-specific T-cell responses, mice of both genotypes were co-housed from birth to the end-point of a four week H. pylori infection
Summary
Arnold & Zhang et al report that CD103+ DCs are required for protective Th1 responses, infection control of mucosal and systemic bacterial pathogens, and antitumor immunity driven by CD4+ Th1 cells and CD8+ T cells. CD103+ DCs further promote the recruitment of Tbet+ peripherally induced Tregs to sites of infection. The results implicate CD103+ DCs in the trafficking of CXCR3+ Tbet+ T-cells to sites of infection and tumorigenesis
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