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PMID:16832056
| Citation |
Bauer, A, Villunger, A, Labi, V, Fischer, SF, Strasser, A, Wagner, H, Schmid, RM and Häcker, G (2006) The NF-kappaB regulator Bcl-3 and the BH3-only proteins Bim and Puma control the death of activated T cells. Proc. Natl. Acad. Sci. U.S.A. 103:10979-84 |
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| Abstract |
Apoptosis of activated T cells is critical for the termination of immune responses. Here we show that adjuvant-stimulated dendritic cells secrete cytokines that prime activated T cells for survival and analyze the roles of the NF-kappaB regulator Bcl-3 and the proapoptotic Bcl-2 family members Bim and Puma. Bcl-3 overexpression increased survival, and activated bcl-3-/- T cells died abnormally rapidly. Cytokines from adjuvant-stimulated dendritic cells induced Bcl-3, but survival through cytokine priming was Bcl-3-independent. Apoptosis inhibition by Bcl-3 involved blockade of Bim activation, because Bim was overactivated in Bcl-3-deficient cells, and Bcl-3 failed to increase survival of bim-/- T cells. However, adjuvants increased survival also in Bim-deficient T cells. This Bim-independent death pathway is at least in part regulated by Puma, as shown by analysis of puma-/- and noxa-/- T cells. IL-1, IL-7, and IL-15 primed T cells for survival even in the absence of Bim or Puma. Our data define interrelations and a Bim-independent pathway to activated T cell death. |
| Links |
PubMed PMC1544160 Online version:10.1073/pnas.0603625103 |
| Keywords |
Adjuvants, Immunologic; Animals; Apoptosis; Apoptosis Regulatory Proteins/deficiency; Apoptosis Regulatory Proteins/genetics; Apoptosis Regulatory Proteins/metabolism; Cells, Cultured; Dendritic Cells/metabolism; Interleukins/pharmacology; Lymphocyte Activation; Membrane Proteins/deficiency; Membrane Proteins/genetics; Membrane Proteins/metabolism; Mice; Mice, Knockout; NF-kappa B/metabolism; Proto-Oncogene Proteins/deficiency; Proto-Oncogene Proteins/genetics; Proto-Oncogene Proteins/metabolism; Solubility; T-Lymphocytes/cytology; T-Lymphocytes/drug effects; T-Lymphocytes/immunology; T-Lymphocytes/metabolism; Transcription Factors; Tumor Suppressor Proteins/deficiency; Tumor Suppressor Proteins/genetics; Tumor Suppressor Proteins/metabolism |
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Significance
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