Transgenic expression of survivin compensates for OX40-deficiency in driving Th2 development and allergic inflammation. Academic Article uri icon


  • 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.

published proceedings

  • Eur J Immunol

author list (cited authors)

  • Lei, F., Song, J., Haque, R., Xiong, X., Fang, D., Wu, Y., ... Song, J.

citation count

  • 12

complete list of authors

  • Lei, Fengyang||Song, Jianyong||Haque, Rizwanul||Xiong, Xiaofang||Fang, Deyu||Wu, Yuzhang||Lens, Susanne MA||Croft, Michael||Song, Jianxun

publication date

  • July 2013