The deficiency of Gαq leads to enhanced T‐cell survival

We have previously reported that Gαq, the α subunit of the Gq protein, had important roles in dendritic cell migration, B‐cell survival and autoimmunity. In this study, we showed that the deficiency of Gαq led to enhanced T‐cell survival. Cultured Gnaq−/− T cells exhibited survival advantages both in medium alone and in the presence of anti‐CD3 stimulation. Gnaq−/− T cells still exhibited a survival advantage when they were cultured in the presence of interleukin (IL)‐2 or IL‐7. Gnaq−/− T cells were more resistant to activation‐induced cell death (AICD) in vitro. The survival advantage of Gnaq−/− T cells was further confirmed by transferring T cells into syngeneic hosts in vivo. Gαq deficiency might promote T‐cell survival by upregulated Bcl‐xL expression and downregulated Fas and FasL expressions. Furthermore, upon T‐cell receptor (TCR) ligation, Akt activity was increased in Gnaq−/− T cells in comparison with wild‐type (WT) T cells. The survival advantage of Gnaq−/− T cells was significantly attenuated after adding Akt inhibitor. Taken together, our data demonstrated a negative role of Gαq in regulating T‐cell survival.