BATF3-dependent dendritic cells drive both effector and regulatory T-cell responses in bacterially infected tissues.
PLoS Pathog
; 15(6): e1007866, 2019 06.
Article
in En
| MEDLINE
| ID: mdl-31188899
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.
Full text:
1
Database:
MEDLINE
Main subject:
Repressor Proteins
/
Tuberculosis
/
Dendritic Cells
/
Helicobacter pylori
/
Helicobacter Infections
/
T-Lymphocytes, Regulatory
/
Basic-Leucine Zipper Transcription Factors
/
Mycobacterium bovis
Type of study:
Prognostic_studies
Limits:
Animals
Language:
En
Journal:
PLoS Pathog
Year:
2019
Type:
Article
Affiliation country:
Switzerland