期刊
JOURNAL OF IMMUNOLOGY
卷 188, 期 12, 页码 6347-6356出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1103781
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资金
- National Institute of Allergy and Infectious Diseases, National Institutes of Health [AI000746]
- MRC [MC_UP_A253_1028] Funding Source: UKRI
- Medical Research Council [MC_UP_A253_1028] Funding Source: researchfish
The regulators of G protein signaling (RGS) protein superfamily negatively controls G protein-coupled receptor signal transduction pathways. RGS16 is enriched in activated/effector T lymphocytes. In this paper, we show that RGS16 constrains pulmonary inflammation by regulating chemokine-induced T cell trafficking in response to challenge with Schistosoma mansoni. Naive Rgs16(-/-) mice were primed for inflammation by accumulation of CCR10(+) T cells in the lung. Upon pathogen exposure, these mice developed more robust granulomatous lung fibrosis than wild-type counterparts. Distinct Th2 or putative Th17 subsets expressing CCR4 or CCR10 accumulated more rapidly in Rgs16(-/-) lungs following challenge and produced proinflammatory cytokines IL-13 and IL-17B. CCR4(+)Rgs16(-/-) Th2 cells migrated excessively to CCL17 and localized aberrantly in challenged lungs. T lymphocytes were partially excluded from lung granulomas in Rgs16(-/-) mice, instead forming peribronchial/perivascular aggregates. Thus, RGS16-mediated confinement of T cells to Schistosome granulomas mitigates widespread cytokine-mediated pulmonary inflammation. The Journal of Immunology, 2012, 188: 6347-6356.
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