| First Author | Shankar SP | Year | 2012 |
| Journal | J Immunol | Volume | 188 |
| Issue | 12 | Pages | 6347-56 |
| PubMed ID | 22593615 | Mgi Jnum | J:188966 |
| Mgi Id | MGI:5442674 | Doi | 10.4049/jimmunol.1103781 |
| Citation | Shankar SP, et al. (2012) RGS16 attenuates pulmonary Th2/Th17 inflammatory responses. J Immunol 188(12):6347-56 |
| abstractText | 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. |
