Format

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

1
Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.
2
Institute of Medical Microbiology, University of Zurich, Zurich, Switzerland.
3
Department of Dermatology, University of Zurich and University Hospital Zurich, Zurich, Switzerland.

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.

Supplemental Content

Full text links

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