Format

Send to

Choose Destination
Nat Immunol. 2015 Aug;16(8):871-9. doi: 10.1038/ni.3224. Epub 2015 Jul 6.

Production of IL-10 by CD4(+) regulatory T cells during the resolution of infection promotes the maturation of memory CD8(+) T cells.

Author information

1
Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA.
2
1] Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA. [2] Howard Hughes Medical Institute, Chevy Chase, Maryland, USA.
3
1] Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA. [2] Department of Pathology, Yale School of Medicine, New Haven, Connecticut, USA. [3] Interdepartmental Program in Computational Biology and Bioinformatics, Yale School of Medicine, New Haven, Connecticut, USA.
4
1] Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA. [2] Department of Internal Medicine (Rheumatology), Yale School of Medicine, New Haven, Connecticut, USA.

Abstract

Memory CD8(+) T cells are critical for host defense upon reexposure to intracellular pathogens. We found that interleukin 10 (IL-10) derived from CD4(+) regulatory T cells (Treg cells) was necessary for the maturation of memory CD8(+) T cells following acute infection with lymphocytic choriomeningitis virus (LCMV). Treg cell-derived IL-10 was most important during the resolution phase, calming inflammation and the activation state of dendritic cells. Adoptive transfer of IL-10-sufficient Treg cells during the resolution phase 'restored' the maturation of memory CD8(+) T cells in IL-10-deficient mice. Our data indicate that Treg cell-derived IL-10 is needed to insulate CD8(+) T cells from inflammatory signals, and reveal that the resolution phase of infection is a critical period that influences the quality and function of developing memory CD8(+) T cells.

PMID:
26147684
PMCID:
PMC4713030
DOI:
10.1038/ni.3224
[Indexed for MEDLINE]
Free PMC Article

Publication types, MeSH terms, Substances, Grant support

Publication types

MeSH terms

Substances

Grant support

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center