| First Author | Zhou W | Year | 2018 |
| Journal | J Immunol | Volume | 201 |
| Issue | 7 | Pages | 1936-1945 |
| PubMed ID | 30127087 | Mgi Jnum | J:265244 |
| Mgi Id | MGI:6199383 | Doi | 10.4049/jimmunol.1700605 |
| Citation | Zhou W, et al. (2018) The PGI2 Analog Cicaprost Inhibits IL-33-Induced Th2 Responses, IL-2 Production, and CD25 Expression in Mouse CD4(+) T Cells. J Immunol 201(7):1936-1945 |
| abstractText | IL-33 has pleiotropic functions in immune responses and promotes the development of allergic diseases and asthma. IL-33 induces Th2 differentiation and enhances type 2 cytokine production by CD4(+) T cells. However, the regulation of IL-33-driven type 2 cytokine responses is not fully defined. In this study, we investigated the effect of PGI2, a lipid mediator formed in the cyclooxygenase pathway of arachidonic acid metabolism, on naive CD4(+) T cell activation, proliferation, and differentiation by IL-33. Using wild-type and PGI2 receptor (IP) knockout mice, we found that the PGI2 analog cicaprost dose-dependently inhibited IL-33-driven IL-4, IL-5, and IL-13 production by CD4(+) T cells in an IP-specific manner. In addition, cicaprost inhibited IL-33-driven IL-2 production and CD25 expression by CD4(+) T cells. Furthermore, IP knockout mice had increased IL-5 and IL-13 responses of CD4(+) T cells to Alternaria sensitization and challenge in mouse lungs. Because IL-33 is critical for Alternaria-induced type 2 responses, these data suggest that PGI2 not only inhibits IL-33-stimulated CD4(+) Th2 cell responses in vitro but also suppresses IL-33-induced Th2 responses caused by protease-containing allergens in vivo. |
