Microbial Colonization Drives Expansion of IL-1 Receptor 1-Expressing and IL-17-Producing γ/δ T Cells
| Autor: | Hachung Chung, Dennis L. Kasper, Jinyou Duan, Erin B. Troy |
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| Rok vydání: | 2010 |
| Předmět: |
Male
Cancer Research MICROBIO T-Lymphocytes medicine.medical_treatment T cell Population Antigen presentation Biology Models Biological Microbiology Article Mice Antigen T-Lymphocyte Subsets Immunology and Microbiology(all) Virology medicine Animals MOLIMMUNO education Receptor Molecular Biology Cell Proliferation Mice Knockout education.field_of_study Innate immune system Bacteria Interleukin-17 Receptors Interleukin-1 Receptors Antigen T-Cell gamma-delta Cell biology Gastrointestinal Tract Mice Inbred C57BL Cytokine medicine.anatomical_structure Immunology Parasitology Interleukin 17 |
| Zdroj: | Cell Host & Microbe. 7:140-150 |
| ISSN: | 1931-3128 |
| DOI: | 10.1016/j.chom.2010.01.005 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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