Clonality and Longevity of CD4+CD28null T Cells Are Associated with Defects in Apoptotic Pathways1
暂无分享,去创建一个
[1] A. Vallejo,et al. Central Role of Thrombospondin-1 in the Activation and Clonal Expansion of Inflammatory T Cells1 , 2000, The Journal of Immunology.
[2] D. Baltimore,et al. Autoimmunity as a consequence of retrovirus-mediated expression of C-FLIP in lymphocytes. , 2009, Immunity.
[3] D. Leroith,et al. T cell receptor-induced activation and apoptosis in cycling human T cells occur throughout the cell cycle. , 1999, Molecular biology of the cell.
[4] P. Krammer. CD95(APO-1/Fas)-mediated apoptosis: live and let die. , 1999, Advances in immunology.
[5] R. Frye,et al. Perturbation of the T-cell repertoire in patients with unstable angina. , 1999, Circulation.
[6] R. Offringa,et al. Immune Escape of Tumors in Vivo by Expression of Cellular Flice-Inhibitory Protein , 1999, The Journal of experimental medicine.
[7] D. Baltimore,et al. Uncoupling IL-2 signals that regulate T cell proliferation, survival, and Fas-mediated activation-induced cell death. , 1999, Immunity.
[8] J. McCune,et al. Direct Evidence for Thymic Function in Adult Humans , 1999, The Journal of experimental medicine.
[9] Ingo Schmitz,et al. Differential Modulation of Apoptosis Sensitivity in CD95 Type I and Type II Cells* , 1999, The Journal of Biological Chemistry.
[10] C. Weyand,et al. T-cell responses in rheumatoid arthritis: systemic abnormalities-local disease. , 1999, Current opinion in rheumatology.
[11] C. Payá,et al. Cell cycle-dependent regulation of FLIP levels and susceptibility to Fas-mediated apoptosis. , 1999, Journal of immunology.
[12] V. Imbert,et al. Duration of STAT5 activation influences the response of interleukin-2 receptor alpha gene to different cytokines. , 1999, European cytokine network.
[13] Y. Goltsev,et al. Tumor necrosis factor receptor and Fas signaling mechanisms. , 1999, Annual review of immunology.
[14] U. Wagner,et al. Perturbation of the T cell repertoire in rheumatoid arthritis. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[15] S. L. Silins,et al. A functional link for major TCR expansions in healthy adults caused by persistent Epstein-Barr virus infection. , 1998, The Journal of clinical investigation.
[16] Wang,et al. Costimulatory molecules in Wegener's granulomatosis (WG): lack of expression of CD28 and preferential up‐regulation of its ligands B7‐1 (CD80) and B7‐2 (CD86) on T cells , 1998, Clinical and experimental immunology.
[17] J. Tschopp,et al. Inhibition of fas death signals by FLIPs. , 1998, Current opinion in immunology.
[18] A. Colombatti,et al. Age-related persistent clonal expansions of CD28(-) cells: phenotypic and molecular TCR analysis reveals both CD4(+) and CD4(+)CD8(+) cells with identical CDR3 sequences. , 1998, Clinical immunology and immunopathology.
[19] A. Vallejo,et al. Resistance to apoptosis and elevated expression of Bcl-2 in clonally expanded CD4+CD28- T cells from rheumatoid arthritis patients. , 1998, Journal of immunology.
[20] J. Tschopp,et al. Biochemical mechanisms of IL-2-regulated Fas-mediated T cell apoptosis. , 1998, Immunity.
[21] A. Abbas,et al. Homeostasis and self-tolerance in the immune system: turning lymphocytes off. , 1998, Science.
[22] A. Vallejo,et al. Aging-related Deficiency of CD28 Expression in CD4+ T Cells Is Associated with the Loss of Gene-specific Nuclear Factor Binding Activity* , 1998, The Journal of Biological Chemistry.
[23] A. Zettl,et al. T cell receptor repertoire in rheumatoid arthritis. , 1998, International reviews of immunology.
[24] B. Trask,et al. MRIT, a novel death-effector domain-containing protein, interacts with caspases and BclXL and initiates cell death. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[25] S. Chen,et al. CLARP, a death effector domain-containing protein interacts with caspase-8 and regulates apoptosis. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[26] S. Srinivasula,et al. FLAME-1, a Novel FADD-like Anti-apoptotic Molecule That Regulates Fas/TNFR1-induced Apoptosis* , 1997, The Journal of Biological Chemistry.
[27] Margot Thome,et al. Inhibition of death receptor signals by cellular FLIP , 1997, Nature.
[28] D. Schaid,et al. Expansion of unusual CD4+ T cells in severe rheumatoid arthritis. , 1997, Arthritis and rheumatism.
[29] D. Goeddel,et al. Casper is a FADD- and caspase-related inducer of apoptosis. , 1997, Immunity.
[30] P. Kourilsky,et al. Expanded CD4+ and CD8+ T cell clones in elderly humans. , 1997, Journal of immunology.
[31] C. Weyand,et al. Co‐stimulatory pathways controlling activation and peripheral tolerance of human CD4+CD28− T cells , 1997, European journal of immunology.
[32] F. Alt,et al. Functional responses and apoptosis of CD25 (IL-2R alpha)-deficient T cells expressing a transgenic antigen receptor. , 1997, Journal of immunology.
[33] G. Nepom,et al. CD11b+CD28-CD4+ human T cells: activation requirements and association with HLA-DR alleles. , 1996, Journal of immunology.
[34] E. Robinet,et al. Human T cells require IL-2 but not G1/S transition to acquire susceptibility to Fas-mediated apoptosis. , 1996, Journal of immunology.
[35] A. Chott,et al. Persistent clonal expansions of peripheral blood CD4+ lymphocytes in chronic inflammatory bowel disease. , 1996, Journal of immunology.
[36] C. Weyand,et al. The Repertoire of CD4+ CD28− T Cells in Rheumatoid Arthritis , 1996, Molecular medicine.
[37] P. Tighe,et al. Restrictions of T cell receptor beta chain repertoire in the peripheral blood of patients with systemic lupus erythematosus. , 1996, Annals of the rheumatic diseases.
[38] P. Carlson,et al. Oligoclonal T cell proliferation in patients with rheumatoid arthritis and their unaffected siblings. , 1996, Arthritis and rheumatism.
[39] A. Theofilopoulos,et al. T cell receptor biases and clonal proliferations among lung transplant recipients with obliterative bronchiolitis. , 1996, The Journal of clinical investigation.
[40] C. Weyand,et al. CD4+ CD7- CD28- T cells are expanded in rheumatoid arthritis and are characterized by autoreactivity. , 1996, The Journal of clinical investigation.
[41] R. Abraham,et al. Interleukin-2 receptor signaling mechanisms. , 1996, Advances in immunology.
[42] F. Ramsdell,et al. Fas and FasL in the homeostatic regulation of immune responses. , 1995, Immunology today.
[43] F. Alt,et al. Interleukin-2 receptor alpha chain regulates the size and content of the peripheral lymphoid compartment. , 1995, Immunity.
[44] D N Posnett,et al. Clonal populations of T cells in normal elderly humans: the T cell equivalent to "benign monoclonal gammapathy" [published erratum appears in J Exp Med 1994 Mar 1;179(3):1077] , 1994, The Journal of experimental medicine.
[45] M. Lenardo,et al. Propriocidal apoptosis of mature T lymphocytes occurs at S phase of the cell cycle , 1993, European journal of immunology.
[46] M. Lenardo. lnterleukin-2 programs mouse αβ T lymphocytes for apoptosis , 1991, Nature.
[47] M. Toribio,et al. lnterleukin-2-dependent autocrine proliferation in T-cell development , 1989, Nature.
[48] M. Toribio,et al. Interleukin-2-dependent autocrine proliferation in T-cell development. , 1989, Nature.
[49] K. Smith,et al. Interleukin-2 induction of T-cell G1 progression and c-myb expression. , 1986, Science.
[50] S. Hickman. Benign monoclonal gammopathy. , 1982, Archives of internal medicine.