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RGS16 Attenuates Pulmonary Th2/Thl7 Inflammatory Responses.
- Source :
-
Journal of Immunology . 6/15/2012, Vol. 188 Issue 12, p6347-6356. 10p. - Publication Year :
- 2012
-
Abstract
- The regulators of Gprotein signaling (RGS) protein superfamily negatively controls Gprotein-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 Rgsl6-/- 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 Thl7 subsets expressing CCR4 or CCR10 accumulated more rapidly in Rgsl6-/- lungs following challenge and produced proinflammatory cytokines IL-13 and IL-17B. CCRA+Rgsl6-/- Th2 cells migrated excessively to CCL17 and localized aberrantly in challenged lungs. T lymphocytes were partially excluded from lung granulomas in Rgsl6-/- mice, instead forming peribronchial/perivascular aggregates. Thus, RGS16-mediated confinement of T cells to Schistosome granulomas mitigates widespread cytokine-mediated pulmonary inflammation. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00221767
- Volume :
- 188
- Issue :
- 12
- Database :
- Academic Search Index
- Journal :
- Journal of Immunology
- Publication Type :
- Academic Journal
- Accession number :
- 77344726
- Full Text :
- https://doi.org/10.4049/jimmunol.1103781