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- W4313387398 abstract "Abstract Schnurri-2 (Shn-2) is a large zinc-finger containing protein, and it plays a critical role in cell growth, signal transduction and lymphocyte development. In Shn-2-deficient CD4 T cells, the activation of NF-kB was upregulated and their ability to differentiate into Th2 cells was enhanced. We herein demonstrate that Th1 and Th2 memory cells are not properly generated from Shn-2-deficient effector Th1/Th2 cells. Even a week after the transfer of effector Th1/Th2 cells into syngeneic mice, a dramatic decrease in the number of Shn-2-deficient donor T cells was detected particularly in the lymphoid organs. The transferred Shn-2-deficient Th1/Th2 cells express higher levels of the activation marker CD69. No significant defect in the BrdU incorporation in the Shn-2-deficient transferred CD4 T cells was observed. The numbers of apoptotic cells were selectively higher in Shn-2-deficient donor Th1/Th2 cell population. Moreover, Shn-2-deficient effector Th1 and Th2 cells showed an increased susceptibility to cell death in in vitro cultures with increased expression of FasL. Transfer of Th2 effector cells over-expressing the p65 subunit of NF-kB resulted in a decreased number of p65-expressing cells in the lymphoid organs. As expected, T cell-dependent antibody responses after in vivo immunization of Shn-2-deficient mice were significantly reduced. Thus, Shn-2 appears to control the generation of memory Th1/Th2 cells through a change in their susceptibility to cell death." @default.
- W4313387398 created "2023-01-06" @default.
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- W4313387398 date "2007-04-01" @default.
- W4313387398 modified "2023-09-27" @default.
- W4313387398 title "Shnurri-2 controls memory Th1 and Th2 cell numbers in vivo (84.3)" @default.
- W4313387398 doi "https://doi.org/10.4049/jimmunol.178.supp.84.3" @default.
- W4313387398 hasPublicationYear "2007" @default.
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