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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


  • Shankar SP
  • Wilson MS
  • DiVietro JA
  • Mentink-Kane MM
  • Xie Z
  • Wynn TA
  • Druey KM


Journal of immunology (Baltimore, Md. : 1950)

Publication Data

June 15, 2012

Associated Grants

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

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