Prostaglandin I2-IP signaling promotes Th1 differentiation in a mouse model of contact hypersensitivity

Saeko Nakajima, Tetsuya Honda, Daiji Sakata, Gyohei Egawa, Hideaki Tanizaki, Atsushi Otsuka, Catharina Sagita Moniaga, Takeshi Watanabe, Yoshiki Miyachi, Shuh Narumiya, Kenji Kabashima

Research output: Contribution to journalArticlepeer-review

56 Citations (Scopus)


PGI2, 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 PGI2-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-γ 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 PGI2 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 PGI2-IP signaling promotes Th1 differentiation through a cAMP-protein kinase A pathway and thereby initiates acquired cutaneous immune responses.

Original languageEnglish
Pages (from-to)5595-5603
Number of pages9
JournalJournal of Immunology
Issue number10
Publication statusPublished - May 15 2010
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology


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