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Cell Host Microbe. 2010 Feb 18;7(2):140-50. doi: 10.1016/j.chom.2010.01.005.

Microbial colonization drives expansion of IL-1 receptor 1-expressing and IL-17-producing gamma/delta T cells.

Author information

1
Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.

Abstract

IL-17 cytokine production by the Th17 T cell subset is regulated by intestinal commmensals. We show that microbial colonization also regulates innate IL-17 production. A population of CD62L(-) gamma/delta T cells, in particular a lineage expressing the IL-1 receptor 1 (IL-1R1), can be quickly activated by microbes to produce IL-17. Antibiotic treatment and monocolonization of mice suggest that specific commensals-but not metronidazole-sensitive anaerobes like Bacteroides species-are required for maintaining IL-1R1(+) gamma/delta T cells. Signaling through the guanine nucleotide exchange factor VAV1, but not through Toll-like receptors or antigen presentation pathways, is essential for inducing IL-1R1(+) gamma/delta T cells. Furthermore, IL-1R1(+) gamma/delta T cells are a potential source of IL-17 that can be activated by IL-23 and IL-1 in both infectious and noninfectious settings in vitro and in vivo. Thus, commensals orchestrate the expansion of phenotypically distinct gammadelta T cells, and innate immunity is a three-way interaction between host, pathogens, and microbiota.

PMID:
20159619
PMCID:
PMC4048034
DOI:
10.1016/j.chom.2010.01.005
[Indexed for MEDLINE]
Free PMC Article

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