title: The deficiency of Gαq leads to enhanced T-cell survival.
abstract: 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.
authors: Molecular Biology Research Center, Shandong Medical College, Linyi, China.
authors: Dashan
authors: D
authors: Wang
authors: Department of Rheumatology, The Affiliated Hospital of Luzhou Medical College, Luzhou, China.
authors: Yugao
authors: Y
authors: Zhang
authors: Department of Rheumatology, The First Affiliated Hospital of Xiamen University, Xiamen, China.
authors: Yan
authors: Y
authors: He
authors: Department of Rheumatology, The First Affiliated Hospital of Xiamen University, Xiamen, China.
authors: Yan
authors: Y
authors: Li
authors: Department of Microbiology, The University of Alabama at Birmingham, Birmingham, AL, USA.
authors: Frances E
authors: FE
authors: Lund
authors: Department of Rheumatology, The First Affiliated Hospital of Xiamen University, Xiamen, China.
authors: Guixiu
authors: G
authors: Shi
mesh_terms: D000818:Animals; D016923:Cell Death / Q000235:genetics / Q000276:immunology; D002470:Cell Survival / Q000235:genetics* / Q000276:immunology*; D015536:Down-Regulation / Q000235:genetics / Q000276:immunology; D053222:Fas Ligand Protein / Q000235:genetics / Q000276:immunology; D043802:GTP-Binding Protein alpha Subunits, Gq-G11 / Q000235:genetics* / Q000276:immunology*; D007376:Interleukin-2 / Q000235:genetics / Q000276:immunology; D015851:Interleukin-7 / Q000235:genetics / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000276:immunology; D011948:Receptors, Antigen, T-Cell / Q000235:genetics / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D015854:Up-Regulation / Q000235:genetics / Q000276:immunology
chemical_list: D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D007376:Interleukin-2; D015851:Interleukin-7; D011948:Receptors, Antigen, T-Cell; D051057:Proto-Oncogene Proteins c-akt; D043802:GTP-Binding Protein alpha Subunits, Gq-G11