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RGS16 attenuates pulmonary Th2/Th17 inflammatory responses.

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.

Pubmed ID: 22593615 RIS Download

Mesh terms: Animals | Chemotaxis, Leukocyte | Cytokines | Flow Cytometry | Immunohistochemistry | Mice | Mice, Inbred C57BL | Mice, Knockout | Pneumonia | RGS Proteins | Real-Time Polymerase Chain Reaction | Schistosomiasis mansoni | Th17 Cells | Th2 Cells

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Associated grants

  • Agency: Medical Research Council, Id: MC_UP_A253_1028
  • Agency: NIAID NIH HHS, Id: Z01 AI000746
  • Agency: Intramural NIH HHS, Id: ZIA AI000746-12

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