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- W4313379023 abstract "Abstract The inhibitor of apoptosis family molecule survivin has been suggested to be a crucial intermediate in 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 increased antigen-driven Th2 lung inflammation, and that constitutive expression of survivin reverses defective lung inflammation in the absence of OX40 costimulation. We found that while OX40-deficient mice are compromised in generating Th2 cells, airway eosinophilia, and IgE responses, survivin transgenic and OX40-deficient mice generate normal Th2 responses and exhibit strong lung inflammation. These data suggest OX40 costimulation crucially engages survivin during antigen-mediated Th2 responses, and promote the notion that targeting survivin could be therapeutically useful for controlling allergic responses or lung inflammation." @default.
- W4313379023 created "2023-01-06" @default.
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- W4313379023 date "2013-05-01" @default.
- W4313379023 modified "2023-09-27" @default.
- W4313379023 title "Transgenic expression of survivin compensates the OX40-deficiency in driving Th2 development and allergic inflammation (P1184)" @default.
- W4313379023 doi "https://doi.org/10.4049/jimmunol.190.supp.190.17" @default.
- W4313379023 hasPublicationYear "2013" @default.
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