| First Author | Lei F | Year | 2013 |
| Journal | Eur J Immunol | Volume | 43 |
| Issue | 7 | Pages | 1914-24 |
| PubMed ID | 23616302 | Mgi Jnum | J:201021 |
| Mgi Id | MGI:5510646 | Doi | 10.1002/eji.201243081 |
| Citation | Lei F, et al. (2013) Transgenic expression of survivin compensates for OX40-deficiency in driving Th2 development and allergic inflammation. Eur J Immunol 43(7):1914-24 |
| abstractText | Survivin, an inhibitor of apoptosis family molecule, has been proposed as a crucial intermediate in the signaling pathways leading to T-cell development, proliferation, and expansion. However, the importance of survivin to T-cell-driven inflammatory responses has not been demonstrated. Here, we show that survivin transgenic mice exhibit an increased antigen-driven Th2 lung inflammation and that constitutive expression of survivin reversed the defective lung inflammation even in the absence of OX40 costimulation. We found that OX40-deficient mice were compromised in generating Th2 cells, airway eosinophilia, and IgE responses. In contrast, OX40-deficient/survivin transgenic mice generated normal Th2 responses and exhibited strong lung inflammation. These results suggest that OX40 costimulation crucially engages survivin during antigen-mediated Th2 responses. These findings also promote the notion that OX40 costimulation regulates allergic responses or lung inflammation by targeting survivin thereby enhancing T-cell proliferation and resulting in more differentiated Th2 cells in the allergic inflammatory response. |
