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Volumn 10, Issue 6, 1998, Pages 669-676

Regulation of autoimmunity by proinflammatory cytokines

Author keywords

[No Author keywords available]

Indexed keywords

CYTOKINE; TUMOR NECROSIS FACTOR ALPHA;

EID: 0032401777     PISSN: 09527915     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0952-7915(98)80087-3     Document Type: Article
Times cited : (129)

References (59)
  • 1
    • 0026717674 scopus 로고
    • The pathophysiology of tumor necrosis factors
    • Vassalli P. The pathophysiology of tumor necrosis factors. Annu Rev Immunol. 10:1992;411-452.
    • (1992) Annu Rev Immunol , vol.10 , pp. 411-452
    • Vassalli, P.1
  • 2
    • 0030769165 scopus 로고    scopus 로고
    • The role of TNFα and related cytokines in the development and function of the autoreactive T-cell repertoire
    • of special interest. This review discusses the possible mechanisms for the apparently paradoxical effects of TNF injections during the neonatal and adult period in NOD mice. The discussion focuses on, firstly, the developmental lymphoid system anomalies arising through chronic TNF blockade and, secondly, the possibility that chronic TNF treatment targets TCR signaling in developing thymocytes during the neonatal period but targets effector T cells in the adult. In thymocytes, attenuation of TCR signaling would impair negative selection of autoreactive T cells and lead to accelerated disease; the same process of suppression would depress effector function in established pathogenic T cells in the adult, leading to disease suppression (see also [10,42]).
    • Cope A, Ettinger R, McDevitt H. The role of TNFα and related cytokines in the development and function of the autoreactive T-cell repertoire. of special interest Res Immunol. 148:1997;307-312 This review discusses the possible mechanisms for the apparently paradoxical effects of TNF injections during the neonatal and adult period in NOD mice. The discussion focuses on, firstly, the developmental lymphoid system anomalies arising through chronic TNF blockade and, secondly, the possibility that chronic TNF treatment targets TCR signaling in developing thymocytes during the neonatal period but targets effector T cells in the adult. In thymocytes, attenuation of TCR signaling would impair negative selection of autoreactive T cells and lead to accelerated disease; the same process of suppression would depress effector function in established pathogenic T cells in the adult, leading to disease suppression (see also [10,42]).
    • (1997) Res Immunol , vol.148 , pp. 307-312
    • Cope, A.1    Ettinger, R.2    McDevitt, H.3
  • 6
    • 0027275490 scopus 로고
    • A novel domain within the 55kd TNF receptor signals cell death
    • Tartaglia LA, Ayres TM, Wong GHW, Goeddel DV. A novel domain within the 55kd TNF receptor signals cell death. Cell. 74:1993;845-853.
    • (1993) Cell , vol.74 , pp. 845-853
    • Tartaglia, L.A.1    Ayres, T.M.2    Wong, G.H.W.3    Goeddel, D.V.4
  • 9
    • 0030200829 scopus 로고    scopus 로고
    • The roles of Fas/APO-1 (CD95) and TNF in antigen-induced programmed cell death in T cell receptor transgenic mice
    • Sytwu HK, Liblau RS, McDevitt HO. The roles of Fas/APO-1 (CD95) and TNF in antigen-induced programmed cell death in T cell receptor transgenic mice. Immunity. 5:1996;17-30.
    • (1996) Immunity , vol.5 , pp. 17-30
    • Sytwu, H.K.1    Liblau, R.S.2    McDevitt, H.O.3
  • 10
    • 0029112641 scopus 로고
    • Cytotoxic effect of TNF and lymphotoxin on T lymphoblasts
    • Sarin A, Conan-Cibotti M, Henkart PA. Cytotoxic effect of TNF and lymphotoxin on T lymphoblasts. J Immunol. 155:1995;3716-3718.
    • (1995) J Immunol , vol.155 , pp. 3716-3718
    • Sarin, A.1    Conan-Cibotti, M.2    Henkart, P.A.3
  • 11
    • 0025875259 scopus 로고
    • Lpr and gld: Single gene models of systemic autoimmunity and lymphoproliferative disease
    • Cohen PL, Eisenberg RA. Lpr and gld: single gene models of systemic autoimmunity and lymphoproliferative disease. Annu Rev Immunol. 9:1991;243-269.
    • (1991) Annu Rev Immunol , vol.9 , pp. 243-269
    • Cohen, P.L.1    Eisenberg, R.A.2
  • 12
    • 0029989339 scopus 로고    scopus 로고
    • Immune and inflammatory responses in TNFα-deficient mice: A central requirement of TNFα in the formation of primary B cell follicular dendritic cell networks and germinal centers, and in the maturation of the humoral immune response
    • Pasparakis M, Alexopoulou L, Episkopou V, Kollias G. Immune and inflammatory responses in TNFα-deficient mice: a central requirement of TNFα in the formation of primary B cell follicular dendritic cell networks and germinal centers, and in the maturation of the humoral immune response. J Exp Med. 184:1996;1397-1411.
    • (1996) J Exp Med , vol.184 , pp. 1397-1411
    • Pasparakis, M.1    Alexopoulou, L.2    Episkopou, V.3    Kollias, G.4
  • 13
    • 0031008477 scopus 로고    scopus 로고
    • Peyer's patch organogenesis is intact yet formation of B lymphocyte follicles is defective in peripheral lymphoid organs of mice deficient for tumor necrosis factor and its 55-kDa receptor
    • Pasparakis M, Alexopoulou L, Grell M, Pfizenmaier K, Bluethmann H, Kollias G. Peyer's patch organogenesis is intact yet formation of B lymphocyte follicles is defective in peripheral lymphoid organs of mice deficient for tumor necrosis factor and its 55-kDa receptor. Proc Natl Acad Sci USA. 94:1997;6319-6323.
    • (1997) Proc Natl Acad Sci USA , vol.94 , pp. 6319-6323
    • Pasparakis, M.1    Alexopoulou, L.2    Grell, M.3    Pfizenmaier, K.4    Bluethmann, H.5    Kollias, G.6
  • 15
    • 0030777295 scopus 로고    scopus 로고
    • Inhibition of T cell apoptosis in the rheumatoid synovium
    • high phenotype, unfractionated synovial fluid T cells from patients with RA fail to undergo apoptosis; neutrophil apoptosis, by contrast, is clearly evident. When removed from the inflammatory environment, purified T cells die if untreated but cells can be rescued - with IL-2, IL-15 or using co-culture with fibroblasts or fibroblast-conditioned meidum. This protection is also integrin mediated. What is intriguing is that defective T cell apoptosis is particular to RA, because no defect can be identified when T cells from patients with gout are studied.
    • high phenotype, unfractionated synovial fluid T cells from patients with RA fail to undergo apoptosis; neutrophil apoptosis, by contrast, is clearly evident. When removed from the inflammatory environment, purified T cells die if untreated but cells can be rescued - with IL-2, IL-15 or using co-culture with fibroblasts or fibroblast-conditioned meidum. This protection is also integrin mediated. What is intriguing is that defective T cell apoptosis is particular to RA, because no defect can be identified when T cells from patients with gout are studied.
    • (1997) J Clin Invest , vol.99 , pp. 439-446
    • Salmon, M.1    Scheel-Toellner, D.2    Huissoon, A.P.3    Pilling, D.4    Shamsadeen, N.5    Hyde, H.6    Dupuy D'Angeac, A.7    Bacon, P.A.8    Emery, P.9    Akbar, A.N.10
  • 17
    • 0031570928 scopus 로고    scopus 로고
    • Inflammatory cytokines enhance the in vivo clonal expansion and differentiation of antigen-activated CD4+ T cells
    • + TCR-transgenic T cells from DO11.10 mice lead to transient accumulation of T cells in lymphoid tissues (as determined with anticlonotypic antibodies) which is increased significantly not only by LPS but also by three consecutive injections of recombinant TNF or IL-1 but not IL-6. These effects are antigen dependent. Adjuvants may work through the same mechanisms.
    • + TCR-transgenic T cells from DO11.10 mice lead to transient accumulation of T cells in lymphoid tissues (as determined with anticlonotypic antibodies) which is increased significantly not only by LPS but also by three consecutive injections of recombinant TNF or IL-1 but not IL-6. These effects are antigen dependent. Adjuvants may work through the same mechanisms.
    • (1997) J Immunol , vol.159 , pp. 591-598
    • Pape, K.A.1    Khoruts, A.2    Mondino, A.3    Jenkins, M.K.4
  • 18
    • 0030298294 scopus 로고    scopus 로고
    • Dissection of TNF receptor 1 effector functions: JNK activation is not linked to apoptosis while NF-κB activation prevents cell death
    • Liu Z-G, Hsu H, Goeddel DV, Karin M. Dissection of TNF receptor 1 effector functions: JNK activation is not linked to apoptosis while NF-κB activation prevents cell death. Cell. 87:1996;565-576.
    • (1996) Cell , vol.87 , pp. 565-576
    • Liu Z-G1    Hsu, H.2    Goeddel, D.V.3    Karin, M.4
  • 19
    • 0029976817 scopus 로고    scopus 로고
    • An essential role for NF-κB in preventing TNF-α-induced cell death
    • Beg AA, Baltimore D. An essential role for NF-κB in preventing TNF-α-induced cell death. Science. 274:1996;782-784.
    • (1996) Science , vol.274 , pp. 782-784
    • Beg, A.A.1    Baltimore, D.2
  • 20
    • 0029858387 scopus 로고    scopus 로고
    • TNF- And cancer therapy-induced apoptosis: Potentiation by inhibition of NF-κB
    • Wang C-Y, Mayo MW, Baldwin AS Jr. TNF- and cancer therapy-induced apoptosis: potentiation by inhibition of NF-κB. Science. 274:1996;784-787.
    • (1996) Science , vol.274 , pp. 784-787
    • Wang C-Y1    Mayo, M.W.2    Baldwin A.S., Jr.3
  • 23
    • 0028289244 scopus 로고
    • Efficient presentation of soluble antigen by cultured human dendritic cells is maintained by granulocyte/macrophage colony-stimulating factor plus interleukin 4 and downregulated by tumor necrosis factor α
    • Sallusto F, Lanzavecchia A. Efficient presentation of soluble antigen by cultured human dendritic cells is maintained by granulocyte/macrophage colony-stimulating factor plus interleukin 4 and downregulated by tumor necrosis factor α J Exp Med. 179:1994;1109-1118.
    • (1994) J Exp Med , vol.179 , pp. 1109-1118
    • Sallusto, F.1    Lanzavecchia, A.2
  • 24
    • 0023874728 scopus 로고
    • Tumour necrosis factor-α In murine autoimmune 'lupus' nephritis
    • Jacob CO, McDevitt HO. Tumour necrosis factor-α in murine autoimmune 'lupus' nephritis. Nature. 331:1988;356-358.
    • (1988) Nature , vol.331 , pp. 356-358
    • Jacob, C.O.1    McDevitt, H.O.2
  • 25
    • 0028081880 scopus 로고
    • Continuous administration of anti-interleukin 10 antibodies delays onset of autoimmunity in NZB/W F1 mice
    • Ishida H, Muchamuel T, Sakaguchi S, Andrade S, Menon S, Howard M. Continuous administration of anti-interleukin 10 antibodies delays onset of autoimmunity in NZB/W F1 mice. J Exp Med. 179:1994;305-310.
    • (1994) J Exp Med , vol.179 , pp. 305-310
    • Ishida, H.1    Muchamuel, T.2    Sakaguchi, S.3    Andrade, S.4    Menon, S.5    Howard, M.6
  • 26
    • 0024341726 scopus 로고
    • Chronic therapy with recombinant tumor necrosis factor-α In autoimmune NZB/W F1 mice
    • Gordon C, Ranges GE, Greenspan JS, Wofsy D. Chronic therapy with recombinant tumor necrosis factor-α in autoimmune NZB/W F1 mice. Clin Immunol Immunopathol. 52:1989;421-434.
    • (1989) Clin Immunol Immunopathol , vol.52 , pp. 421-434
    • Gordon, C.1    Ranges, G.E.2    Greenspan, J.S.3    Wofsy, D.4
  • 27
    • 0030584786 scopus 로고    scopus 로고
    • Greatly accelerated lymphadenopathy and autoimmune disease in lpr mice lacking tumor necrosis factor receptor 1
    • Zhou T, Edwards CK, Yang P, Wang Z, Bluethmann H, Mountz JD. Greatly accelerated lymphadenopathy and autoimmune disease in lpr mice lacking tumor necrosis factor receptor 1. J Immunol. 156:1996;2661-2665.
    • (1996) J Immunol , vol.156 , pp. 2661-2665
    • Zhou, T.1    Edwards, C.K.2    Yang, P.3    Wang, Z.4    Bluethmann, H.5    Mountz, J.D.6
  • 28
    • 0025360026 scopus 로고
    • Effects of recombinant murine tumor necrosis factor-α On immune function
    • Gordon C, Wofsy D. Effects of recombinant murine tumor necrosis factor-α on immune function. J Immunol. 144:1990;1753-1758.
    • (1990) J Immunol , vol.144 , pp. 1753-1758
    • Gordon, C.1    Wofsy, D.2
  • 29
    • 0027978457 scopus 로고
    • Chronic exposure to tumor necrosis factor (TNF) in vitro impairs the activation of T cells through the T cell receptor/CD3 complex; Reversal in vivo by anti-TNF antibodies in patients with rheumatoid arthritis
    • Cope AP, Londei M, Chu NR, Cohen SB, Elliott MJ, Brennan FM, Maini RN, Feldmann M. Chronic exposure to tumor necrosis factor (TNF) in vitro impairs the activation of T cells through the T cell receptor/CD3 complex; reversal in vivo by anti-TNF antibodies in patients with rheumatoid arthritis. J Clin Invest. 94:1994;749-760.
    • (1994) J Clin Invest , vol.94 , pp. 749-760
    • Cope, A.P.1    Londei, M.2    Chu, N.R.3    Cohen, S.B.4    Elliott, M.J.5    Brennan, F.M.6    Maini, R.N.7    Feldmann, M.8
  • 30
    • 0029671297 scopus 로고    scopus 로고
    • In vivo blockade of TNF-alpha by intravenous infusion of a chimeric monoclonal TNF-alpha antibody in patients with rheumatoid arthritis. Short term cellular and molecular effects
    • Lorenz HM, Antoni C, Valerius T, Repp R, Grunke M, Schwerdtner N, Nusslein H, Woody J, Kalden JR, Manger B. In vivo blockade of TNF-alpha by intravenous infusion of a chimeric monoclonal TNF-alpha antibody in patients with rheumatoid arthritis. Short term cellular and molecular effects. J Immunol. 156:1996;1646-1653.
    • (1996) J Immunol , vol.156 , pp. 1646-1653
    • Lorenz, H.M.1    Antoni, C.2    Valerius, T.3    Repp, R.4    Grunke, M.5    Schwerdtner, N.6    Nusslein, H.7    Woody, J.8    Kalden, J.R.9    Manger, B.10
  • 31
    • 0029559439 scopus 로고
    • Role of tumor necrosis factor-α In the regulation of activated synovial T cell growth: Downregulation of synovial T cells in rheumatoid arthritis
    • Lai N-S, Lan J-L, Yu C-L, Lin R-H. Role of tumor necrosis factor-α in the regulation of activated synovial T cell growth: downregulation of synovial T cells in rheumatoid arthritis. Eur J Immunol. 25:1995;3243-3248.
    • (1995) Eur J Immunol , vol.25 , pp. 3243-3248
    • Lai N-S1    Lan J-L2    Yu C-L3    Lin R-H4
  • 32
    • 0030911341 scopus 로고    scopus 로고
    • Chronic tumor necrosis factor alters T cell responses by attenuating T cell receptor signaling
    • of special interest. This series of experiments examines the function of TCR-transgenic T cells exposed to TNF for prolonged periods in vitro or in vivo, following stimulation with specific peptide. The results show that chronic TNF effects are dose- and time-dependent; Th1 and Th2 responses are impaired; effects are reversible with anti-TNF antibodies; and chronic TNF attenuates early TCR signaling events. Peptide-specific responses are also depressed in TCR x human TNF-globin double-transgenic mice, implying a role for sustained signaling via the p55 TNF-R. Interestingly, the effects in B10.D2 and Balb/c strains are different.
    • Cope AP, Liblau RS, Yang XD, Congia M, Laudanna C, Schreiber RD, Probert L, Kollias G, McDevitt HO. Chronic tumor necrosis factor alters T cell responses by attenuating T cell receptor signaling. of special interest J Exp Med. 185:1997;1573-1584 This series of experiments examines the function of TCR-transgenic T cells exposed to TNF for prolonged periods in vitro or in vivo, following stimulation with specific peptide. The results show that chronic TNF effects are dose- and time-dependent; Th1 and Th2 responses are impaired; effects are reversible with anti-TNF antibodies; and chronic TNF attenuates early TCR signaling events. Peptide-specific responses are also depressed in TCR x human TNF-globin double-transgenic mice, implying a role for sustained signaling via the p55 TNF-R. Interestingly, the effects in B10.D2 and Balb/c strains are different.
    • (1997) J Exp Med , vol.185 , pp. 1573-1584
    • Cope, A.P.1    Liblau, R.S.2    Yang, X.D.3    Congia, M.4    Laudanna, C.5    Schreiber, R.D.6    Probert, L.7    Kollias, G.8    McDevitt, H.O.9
  • 33
    • 0029834839 scopus 로고    scopus 로고
    • Local expression of transgene encoded TNF alpha in islets prevents autoimmune diabetes in nonobese diabetic (NOD) mice by preventing the development of auto-reactive islet-specific T cells
    • Grewal IS, Grewal KD, Wong FS, Picarella DE, Janeway CA Jr, Flavell RA. Local expression of transgene encoded TNF alpha in islets prevents autoimmune diabetes in nonobese diabetic (NOD) mice by preventing the development of auto-reactive islet-specific T cells. J Exp Med. 184:1996;1963-1974.
    • (1996) J Exp Med , vol.184 , pp. 1963-1974
    • Grewal, I.S.1    Grewal, K.D.2    Wong, F.S.3    Picarella, D.E.4    Janeway C.A., Jr.5    Flavell, R.A.6
  • 35
    • 0028568369 scopus 로고
    • Local production of human IL-6 promotes insulitis but retards the onset of insulin-dependent diabetes mellitus in non-obese diabetic mice
    • DiCosmo BF, Picarella D, Flavell RA. Local production of human IL-6 promotes insulitis but retards the onset of insulin-dependent diabetes mellitus in non-obese diabetic mice. Int Immunol. 6:1994;1829-1837.
    • (1994) Int Immunol , vol.6 , pp. 1829-1837
    • Dicosmo, B.F.1    Picarella, D.2    Flavell, R.A.3
  • 36
    • 0031058726 scopus 로고    scopus 로고
    • Interleukin (IL)-6 directs the differentiation of IL-4-producing CD4+ T cells
    • of special interest. Since macrophage-derived IL-12 production is thought to be pivotal in initiating the differentiation of Th1 cells (together with IFN-γ), the authors examine whether macrophage products could also be responsible for providing analogous signals to Th2 precursors to induce IL-4 production. Their hypothesis is substantiated with regard to IL-6 by experiments using anti-IL-6 or anti-IL-6-R mAbs and in experiments where Il-6 can restore IL-4 production by T cells from IL-6-deficient mice. Interestingly, data indicate that IL-6 induces IL-4 gene expression; this possibly occurs through the presence - in the IL-4 gene 5′ region - of functional binding sites for CCAAT/enhancer-binding protein (C/EBP)-like transcription factors, which include the nuclear factor for IL-6 (NF-IL-6).
    • Rincon M, Anguita J, Nakamura T, Fikrig E, Flavell RA. Interleukin (IL)-6 directs the differentiation of IL-4-producing CD4+ T cells. of special interest J Exp Med. 185:1997;461-469 Since macrophage-derived IL-12 production is thought to be pivotal in initiating the differentiation of Th1 cells (together with IFN-γ), the authors examine whether macrophage products could also be responsible for providing analogous signals to Th2 precursors to induce IL-4 production. Their hypothesis is substantiated with regard to IL-6 by experiments using anti-IL-6 or anti-IL-6-R mAbs and in experiments where Il-6 can restore IL-4 production by T cells from IL-6-deficient mice. Interestingly, data indicate that IL-6 induces IL-4 gene expression; this possibly occurs through the presence - in the IL-4 gene 5′ region - of functional binding sites for CCAAT/enhancer-binding protein (C/EBP)-like transcription factors, which include the nuclear factor for IL-6 (NF-IL-6).
    • (1997) J Exp Med , vol.185 , pp. 461-469
    • Rincon, M.1    Anguita, J.2    Nakamura, T.3    Fikrig, E.4    Flavell, R.A.5
  • 37
    • 0031571717 scopus 로고    scopus 로고
    • Defective TCR-mediated signaling in synovial T cells in rheumatoid arthritis
    • 2+ fluxing is impaired in T cells from RA patients following TCR/CD3 ligation, the authors demonstrate convincingly that activation-induced tyrosine phosphorylation is impaired in synovial T cells; this most notably affects the p38 phosphoprotein but also the TCRζ chain, whose expression is also reduced. CD3ε expression is spared. The intriguing link between redox status and TCRζ chain expression is discussed.
    • 2+ fluxing is impaired in T cells from RA patients following TCR/CD3 ligation, the authors demonstrate convincingly that activation-induced tyrosine phosphorylation is impaired in synovial T cells; this most notably affects the p38 phosphoprotein but also the TCRζ chain, whose expression is also reduced. CD3ε expression is spared. The intriguing link between redox status and TCRζ chain expression is discussed.
    • (1997) J Immunol , vol.159 , pp. 2973-2978
    • Maurice, M.M.1    Lankester, A.C.2    Bezemer, A.C.3    Geertsma, M.F.4    Tak, P.P.5    Breedveld, F.C.6    Van Lier, R.A.7    Verweij, C.L.8
  • 38
    • 0031916192 scopus 로고    scopus 로고
    • TNF is a potent anti-inflammatory cytokine in autoimmune-mediated demyelination
    • of outstanding interest. This study, together with [14], provides unequivocal evidence that TNF, though not obligatory for disease induction, has potent anti-inflammatory effects in autoimmune and inflammatory responses that appear to be mediated through p55 TNF-R. Presumably lymphotoxin (LT) cannot compensate, nor is responsible, because anti-LT antibodies do not influence the disease phenotype. The striking observation is that the TNF-null mutation converts a resistant strain to a susceptible one.
    • Liu J, Marino MW, Wong G, Grail D, Dunn A, Bettadapura J, Slavin AJ, Old L, Bernard CC. TNF is a potent anti-inflammatory cytokine in autoimmune-mediated demyelination. of outstanding interest Nat Med. 4:1998;78-83 This study, together with [14], provides unequivocal evidence that TNF, though not obligatory for disease induction, has potent anti-inflammatory effects in autoimmune and inflammatory responses that appear to be mediated through p55 TNF-R. Presumably lymphotoxin (LT) cannot compensate, nor is responsible, because anti-LT antibodies do not influence the disease phenotype. The striking observation is that the TNF-null mutation converts a resistant strain to a susceptible one.
    • (1998) Nat Med , vol.4 , pp. 78-83
    • Liu, J.1    Marino, M.W.2    Wong, G.3    Grail, D.4    Dunn, A.5    Bettadapura, J.6    Slavin, A.J.7    Old, L.8    Bernard, C.C.9
  • 43
    • 0030701533 scopus 로고    scopus 로고
    • Immune complexes are potent inhibitors of interleukin-12 secretion by human monocytes
    • Berger S, Chandra R, Ballo H, Hildenbrand R, Stutte HJ. Immune complexes are potent inhibitors of interleukin-12 secretion by human monocytes. Eur J Immunol. 27:1997;2994-3000.
    • (1997) Eur J Immunol , vol.27 , pp. 2994-3000
    • Berger, S.1    Chandra, R.2    Ballo, H.3    Hildenbrand, R.4    Stutte, H.J.5
  • 45
    • 0031059468 scopus 로고    scopus 로고
    • Regulatory mechanisms that modulate signalling by G-protein-coupled receptors
    • of special interest. This is a comprehensive and detailed review which focuses on the principal mechanisms by which signaling through G-protein-coupled receptors such as neurotransmitters, chemokines and prostanoids can be attenuated.
    • Bohm SK, Grady EF, Bunnett NW. Regulatory mechanisms that modulate signalling by G-protein-coupled receptors. of special interest Biochem J. 322:1997;1-18 This is a comprehensive and detailed review which focuses on the principal mechanisms by which signaling through G-protein-coupled receptors such as neurotransmitters, chemokines and prostanoids can be attenuated.
    • (1997) Biochem J , vol.322 , pp. 1-18
    • Bohm, S.K.1    Grady, E.F.2    Bunnett, N.W.3
  • 48
    • 0028968301 scopus 로고
    • Soluble TNF receptor production by activated T lymphocytes: Differential effects of acute and chronic exposure to TNF
    • Cope AP, Aderka D, Wallach D, Kahan M, Chu NR, Brennan FM, Feldmann M. Soluble TNF receptor production by activated T lymphocytes: differential effects of acute and chronic exposure to TNF. Immunology. 84:1995;21-30.
    • (1995) Immunology , vol.84 , pp. 21-30
    • Cope, A.P.1    Aderka, D.2    Wallach, D.3    Kahan, M.4    Chu, N.R.5    Brennan, F.M.6    Feldmann, M.7
  • 49
    • 0031441901 scopus 로고    scopus 로고
    • Antiproliferative action of interferon-alpha requires components of T-cell-receptor signalling
    • of outstanding interest. Although IFN receptors signal through the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signal transduction pathways, this illuminating study demonstrates that the mechanism for the growth-suppressing effects of IFN-α on human peripheral blood T cells or Jurkat cells involves the sequential recruitment of CD45, lck and ZAP-70 to the IFN-R complex. Consistent with this, Jurkat cells with defective CD45, lck or ZAP-70 are resistant to IFN-α-mediated inhibitory effects, while JAK/STAT and antiviral responses are preserved in these mutants.
    • Petricoin EF III, Ito S, Williams BL, Audet S, Stancato LF, Gamero A, Clouse K, Grimley P, Weiss A, Beeler J, et al. Antiproliferative action of interferon-alpha requires components of T-cell-receptor signalling. of outstanding interest Nature. 390:1997;629-632 Although IFN receptors signal through the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signal transduction pathways, this illuminating study demonstrates that the mechanism for the growth-suppressing effects of IFN-α on human peripheral blood T cells or Jurkat cells involves the sequential recruitment of CD45, lck and ZAP-70 to the IFN-R complex. Consistent with this, Jurkat cells with defective CD45, lck or ZAP-70 are resistant to IFN-α-mediated inhibitory effects, while JAK/STAT and antiviral responses are preserved in these mutants.
    • (1997) Nature , vol.390 , pp. 629-632
    • Petricoin E.F. III1    Ito, S.2    Williams, B.L.3    Audet, S.4    Stancato, L.F.5    Gamero, A.6    Clouse, K.7    Grimley, P.8    Weiss, A.9    Beeler, J.10
  • 50
    • 0029787410 scopus 로고    scopus 로고
    • RANTES induces tyrosine kinase activity of stably complexed p125FAK and ZAP-70 in human T cells
    • Bacon KB, Szabo MC, Yssel H, Bolen JB, Schall TJ. RANTES induces tyrosine kinase activity of stably complexed p125FAK and ZAP-70 in human T cells. J Exp Med. 184:1996;873-882.
    • (1996) J Exp Med , vol.184 , pp. 873-882
    • Bacon, K.B.1    Szabo, M.C.2    Yssel, H.3    Bolen, J.B.4    Schall, T.J.5
  • 51
    • 0025020303 scopus 로고
    • Prevention of diabetes in nonobese diabetic mice by tumor necrosis factor (TNF): Similarities between TNF-alpha and interleukin 1
    • Jacob CO, Aiso S, Michie SA, McDevitt HO, Acha-Orbea H. Prevention of diabetes in nonobese diabetic mice by tumor necrosis factor (TNF): similarities between TNF-alpha and interleukin 1. Proc Natl Acad Sci USA. 87:1990;968-972.
    • (1990) Proc Natl Acad Sci USA , vol.87 , pp. 968-972
    • Jacob, C.O.1    Aiso, S.2    Michie, S.A.3    McDevitt, H.O.4    Acha-Orbea, H.5
  • 52
    • 0032036481 scopus 로고    scopus 로고
    • Altered pattern of TCR/CD3-mediated protein-tyrosyl phosphorylation in T cells from patients with systemic lupus erythematosus. Deficient expression of the T cell receptor zeta chain
    • 2+ fluxing by TCRξ-negative T cells is still higher than responses from control subjects. The patterns of responses defined in prospective studies are independent of drug treatment or disease activity, suggesting that the defect may be genetic - possibly linked to the locus for TCRξ on chromosome 1.
    • 2+ fluxing by TCRξ-negative T cells is still higher than responses from control subjects. The patterns of responses defined in prospective studies are independent of drug treatment or disease activity, suggesting that the defect may be genetic - possibly linked to the locus for TCRξ on chromosome 1.
    • (1998) J Clin Invest , vol.101 , pp. 1448-1457
    • Liossis, S.N.1    Ding, X.Z.2    Dennis, G.J.3    Tsokos, G.C.4
  • 54
    • 0030061922 scopus 로고    scopus 로고
    • IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- And obesity-induced insulin resistance
    • Hotamisligil GS, Peraldi P, Budavari A, Ellis R, White MF, Spiegelman BM. IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance. Science. 271:1996;665-668.
    • (1996) Science , vol.271 , pp. 665-668
    • Hotamisligil, G.S.1    Peraldi, P.2    Budavari, A.3    Ellis, R.4    White, M.F.5    Spiegelman, B.M.6
  • 56
    • 0026525810 scopus 로고
    • Monoclonal anti-tumor necrosis factor antibody renders non-obese diabetic mice hypersensitive to irradiation and enhances insulitis development
    • Jacob CO, Aiso S, Schreiber RD, McDevitt HO. Monoclonal anti-tumor necrosis factor antibody renders non-obese diabetic mice hypersensitive to irradiation and enhances insulitis development. Int Immunol. 4:1992;611-614.
    • (1992) Int Immunol , vol.4 , pp. 611-614
    • Jacob, C.O.1    Aiso, S.2    Schreiber, R.D.3    McDevitt, H.O.4
  • 58
    • 0026474808 scopus 로고
    • Expression of a tumor necrosis factor alpha transgene in murine pancreatic beta cells results in severe and permanent insulitis without evolution towards diabetes
    • Higuchi Y, Herrera P, Muniesa P, Huarte J, Belin D, Ohashi P, Aichele P, Orci L, Vassalli JD, Vassalli P. Expression of a tumor necrosis factor alpha transgene in murine pancreatic beta cells results in severe and permanent insulitis without evolution towards diabetes. J Exp Med. 176:1992;1719-1731.
    • (1992) J Exp Med , vol.176 , pp. 1719-1731
    • Higuchi, Y.1    Herrera, P.2    Muniesa, P.3    Huarte, J.4    Belin, D.5    Ohashi, P.6    Aichele, P.7    Orci, L.8    Vassalli, J.D.9    Vassalli, P.10
  • 59
    • 0027207669 scopus 로고
    • Transgenic tumor necrosis factor (TNF)-alpha production in pancreatic islets leads to insulitis, not diabetes. Distinct patterns of inflammation in TNF-alpha and TNF-beta transgenic mice
    • Picarella DE, Kratz A, Li CB, Ruddle NH, Flavell RA. Transgenic tumor necrosis factor (TNF)-alpha production in pancreatic islets leads to insulitis, not diabetes. Distinct patterns of inflammation in TNF-alpha and TNF-beta transgenic mice. J Immunol. 150:1993;4136-4150.
    • (1993) J Immunol , vol.150 , pp. 4136-4150
    • Picarella, D.E.1    Kratz, A.2    Li, C.B.3    Ruddle, N.H.4    Flavell, R.A.5


* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.