Giannattasio, Giorgio (2010) THE P2Y6 RECEPTOR INHIBITS EFFECTOR T CELL ACTIVATION IN ALLERGIC PULMONARY INFLAMMATION. [Tesi di dottorato] (Inedito)
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| Tipologia del documento: | Tesi di dottorato |
|---|---|
| Lingua: | English |
| Titolo: | THE P2Y6 RECEPTOR INHIBITS EFFECTOR T CELL ACTIVATION IN ALLERGIC PULMONARY INFLAMMATION |
| Autori: | Autore Email Giannattasio, Giorgio giorgionap@yahoo.it |
| Data: | 30 Novembre 2010 |
| Numero di pagine: | 74 |
| Istituzione: | Università degli Studi di Napoli Federico II |
| Dipartimento: | Medicina clinica e scienze cardiovascolari e immunologiche |
| Scuola di dottorato: | Medicina clinica e sperimentale |
| Dottorato: | Fisiopatologia clinica e medicina sperimentale |
| Ciclo di dottorato: | 23 |
| Coordinatore del Corso di dottorato: | nome email Marone, Gianni marone@unina.it |
| Tutor: | nome email Marone, Gianni marone@unina.it |
| Data: | 30 Novembre 2010 |
| Numero di pagine: | 74 |
| Parole chiave: | Purinergic receptor, Allergic inflammation, T cells |
| Settori scientifico-disciplinari del MIUR: | Area 06 - Scienze mediche > MED/09 - Medicina interna |
| Depositato il: | 03 Dic 2010 09:26 |
| Ultima modifica: | 30 Apr 2014 19:46 |
| URI: | http://www.fedoa.unina.it/id/eprint/8384 |
| DOI: | 10.6092/UNINA/FEDOA/8384 |
Abstract
We show that the P2Y6 receptor, a G-protein-coupled receptor with high affinity for the nucleotide uridine diphosphate, is an important endogenous inhibitor of T cell function in allergic pulmonary inflammation. Mice conditionally deficient in P2Y6 receptors [p2ry6 (flox/flox);cre/+ mice] exhibited severe airway and tissue pathology relative to P2Y6-sufficient [p2ry6 (flox/flox)] littermates (+/+ mice) when treated intranasally with an extract (Df) of the dust mite Dermatophagoides farinae. P2Y6 receptors were inducibly expressed by lung, lymph node and splenic CD4+ and CD8+ T cells of Df-treated +/+ mice. Df-restimulated P2Y6-deficient lymph node cells produced higher levels of Th1 and Th2 cytokines, and polyclonally-stimulated P2Y6-deficient CD4+ T cells proliferated faster than comparably stimulated P2Y6-sufficient cells. The absence of P2Y6 receptors on CD4+ cells, but not antigen presenting cells, was sufficient to amplify cytokine generation. Thus, P2Y6 receptors protect the lung against exuberant allergen-induced pulmonary inflammation by inhibiting the activation of effector T cells.
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