Send to

Choose Destination
PLoS Pathog. 2019 Jun 12;15(6):e1007866. doi: 10.1371/journal.ppat.1007866. eCollection 2019 Jun.

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

Author information

Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.
Institute of Medical Microbiology, University of Zurich, Zurich, Switzerland.
Department of Dermatology, University of Zurich and University Hospital Zurich, Zurich, Switzerland.


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.

Supplemental Content

Full text links

Icon for Public Library of Science Icon for PubMed Central
Loading ...
Support Center