| First Author | Nakajima S | Year | 2010 |
| Journal | J Immunol | Volume | 184 |
| Issue | 10 | Pages | 5595-603 |
| PubMed ID | 20400695 | Mgi Jnum | J:160998 |
| Mgi Id | MGI:4456921 | Doi | 10.4049/jimmunol.0903260 |
| Citation | Nakajima S, et al. (2010) Prostaglandin I2-IP signaling promotes Th1 differentiation in a mouse model of contact hypersensitivity. J Immunol 184(10):5595-603 |
| abstractText | PGI(2), which exerts its actions via its specific Gs-coupled I prostanoid receptor (IP), is known to be present in the lymph nodes, but its roles in acquired cutaneous immune responses remain unclear. To investigate the role of PGI(2)-IP signaling in cutaneous immune responses, we applied IP-deficient (Ptgir(-/-)) mice to contact hypersensitivity as a model of acquired immune response and found that Ptgir(-/-) mice exhibited a significantly decreased contact hypersensitivity response. Lymph node cells from sensitized Ptgir(-/-) mice exhibited decreased IFN-gamma production and a smaller T-bet(+) subset compared with control mice. PGI synthase and IP expression were detected in dendritic cells and T cells, respectively, by quantitative real-time PCR analysis, suggesting that PGI(2) produced by dendritic cells acts on IP in T cells. In fact, in vitro Th1 differentiation was enhanced by an IP agonist, and this enhancement was nullified by protein kinase A inhibitor. These results suggest that PGI(2)-IP signaling promotes Th1 differentiation through a cAMP-protein kinase A pathway and thereby initiates acquired cutaneous immune responses. |
