| First Author | Giannattasio G | Year | 2011 |
| Journal | J Immunol | Volume | 187 |
| Issue | 3 | Pages | 1486-95 |
| PubMed ID | 21724990 | Mgi Jnum | J:179177 |
| Mgi Id | MGI:5301234 | Doi | 10.4049/jimmunol.1003669 |
| Citation | Giannattasio G, et al. (2011) The purinergic G protein-coupled receptor 6 inhibits effector T cell activation in allergic pulmonary inflammation. J Immunol 187(3):1486-95 |
| abstractText | We show that the P2Y(6) receptor, a purinergic G protein-coupled receptor with a high affinity for the nucleotide uridine diphosphate, is an important endogenous inhibitor of T cell function in allergic pulmonary inflammation. Mice conditionally deficient in P2Y(6) receptors [p2ry6 (flox/flox);cre/+ mice] exhibited severe airway and tissue pathology relative to P2Y(6)-sufficient [p2ry6 (flox/flox)] littermates (+/+ mice) when treated intranasally with an extract of the dust mite Dermatophagoides farinae (Df). P2Y(6) receptors were inducibly expressed by lung, lymph node, and splenic CD4(+) and CD8(+) T cells of Df-treated +/+ mice. Df-restimulated P2Y(6)-deficient lymph node cells produced higher levels of Th1 and Th2 cytokines, and polyclonally stimulated P2Y(6)-deficient CD4(+) T cells proliferated faster than comparably stimulated P2Y(6)-sufficient cells. The absence of P2Y(6) receptors on CD4(+) cells, but not APCs, was sufficient to amplify cytokine generation. Thus, P2Y(6) receptors protect the lung against exuberant allergen-induced pulmonary inflammation by inhibiting the activation of effector T cells. |
