Acid Sphingomyelinase Is Required for Protection of Effector Memory T Cells against Glucocorticoid-Induced Cell Death
Denise Tischner, Jennifer Theiss, Anna Karabinskaya, Jens van den Brandt, Sybille D Reichardt, Ulrike Karow, Marco J Herold, Fred Luehder, Olaf Utermoehlen, Holger M Reichardt
The Journal of Immunology | AMER ASSOC IMMUNOLOGISTS | Published : 2011
The activity of acid sphingomyelinase (aSMase) was previously reported to be involved in glucocorticoid-induced cell death (GICD) of T lymphocytes. This mechanism in turn is believed to contribute to the therapeutic efficacy of glucocorticoids (GCs) in the treatment of inflammatory diseases. In this study, we reassessed the role of aSMase in GICD by using aSMase knockout mice. The absence of aSMase largely abolished the partial protection that effector memory CD4(+) T cells in wild-type mice possess against GICD. Reduced IL-2 secretion by aSMase-deficient CD4(+) T cells suggested that a lack of this important survival factor might be the cause of these cells' enhanced susceptibility to GICD...View full abstract
Awarded by Deutsche Krebshilfe
Awarded by Deutsche Forschungsgemeinschaft
This work was supported by grants from Deutsche Krebshilfe (108713) and Deutsche Forschungsgemeinschaft (RE 1631/7-1 and LU 638/8-1).