Journal ArticleDOI
The Fas Death Factor
Shigekazu Nagata,Pierre Golstein +1 more
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TLDR
Fas ligand (FasL), a cell surface molecule belonging to the tumor necrosis factor family, binds to its receptor Fas, thus inducing apoptosis of Fas-bearing cells.Abstract:
Fas ligand (FasL), a cell surface molecule belonging to the tumor necrosis factor family, binds to its receptor Fas, thus inducing apoptosis of Fas-bearing cells. Various cells express Fas, whereas FasL is expressed predominantly in activated T cells. In the immune system, Fas and FasL are involved in down-regulation of immune reactions as well as in T cell-mediated cytotoxicity. Malfunction of the Fas system causes lymphoproliferative disorders and accelerates autoimmune diseases, whereas its exacerbation may cause tissue destruction.read more
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Apoptosis by death factor.
TL;DR: This work was supported in part by Grants-in-Aid from the Ministry of Education, Science, and Culture of Japan and by a Research Grant from the Princess Takamatsu Cancer Research Fund, and performed in part through Special Coordination Funds of the Science and Technology Agency of the Japanese Government.
Journal ArticleDOI
Tumor-associated B7-H1 promotes T-cell apoptosis: a potential mechanism of immune evasion
Haidong Dong,Scott E. Strome,Diva R. Salomao,Hideto Tamura,Fumiya Hirano,Dallas B. Flies,Patrick C. Roche,Jun Lu,Gefeng Zhu,Koji Tamada,Vanda A. Lennon,Esteban Celis,Lieping Chen +12 more
TL;DR: It is reported here that, except for cells of the macrophage lineage, normal human tissues do not express B7-H1 and the findings have implications for the design of T cell–based cancer immunotherapy.
Journal ArticleDOI
The TNF and TNF receptor superfamilies: integrating mammalian biology.
TL;DR: The authors regret the inability to cite all of the primary literature contributing to this review due to length considerations, but wish to thank F. Chan, T. Migone, and J. Wang for insightful comments on the manuscript.
Journal ArticleDOI
A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD
Masato Enari,Hideki Sakahira,Hideki Yokoyama,Katsuya Okawa,Akihiro Iwamatsu,Shigekazu Nagata,Shigekazu Nagata +6 more
TL;DR: A caspase-activated deoxyribonuclease (CAD) and its inhibitor (ICAD) have now been identified in the cytoplasmic fraction of mouse lymphoma cells and seems to function as a chaperone for CAD during its synthesis, remaining complexed with CAD to inhibit its DNase activity.
Journal ArticleDOI
FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death--inducing signaling complex.
Marta Muzio,Arul M. Chinnaiyan,Frank C. Kischkel,Karen O'Rourke,Andrej Shevchenko,Jian Ni,Carsten Scaffidi,James D. Bretz,Mei Zhang,Reiner L. Gentz,Matthias Mann,Peter H. Krammer,Marcus E. Peter,Vishva M. Dixit +13 more
TL;DR: This work utilized nano-electrospray tandem mass spectrometry to identify CAP3 and CAP4, components of the CD95 (Fas/APO-1) death-inducing signaling complex, and found a novel 55 kDa protein, designated FLICE, which has homology to both FADD and the ICE/CED-3 family of cysteine proteases.
References
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Journal Article
Effect of bcl-2 on fas antigen-mediated cell death
TL;DR: The results suggest that the Fas Ag and TNF receptor may share the same signaling pathway, and that bcl-2 interferes with the apoptotic process mediated by the FasAg and T NF receptor.
Journal ArticleDOI
Mechanisms of class I restricted immunopathology. A transgenic mouse model of fulminant hepatitis.
Kazuki Ando,Takashi Moriyama,Luca G. Guidotti,Susanne Wirth,R. D. Schreiber,H J Schlicht,Shao-Nan Huang,Francis V. Chisari +7 more
TL;DR: The principles illustrated in this study are generally applicable to other models of class I-restricted, CTL-induced immunopathology, and it is suggested that they contribute to the immunopathogenesis of viral hepatitis during hepatitis B virus infection in humans.
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The role of nitric oxide in the pathogenesis of spontaneous murine autoimmune disease: increased nitric oxide production and nitric oxide synthase expression in MRL-lpr/lpr mice, and reduction of spontaneous glomerulonephritis and arthritis by orally administered NG-monomethyl-L-arginine.
J B Weinberg,D L Granger,David S. Pisetsky,M F Seldin,Mary A. Misukonis,S N Mason,A M Pippen,P Ruiz,E R Wood,Gary S. Gilkeson +9 more
TL;DR: The results suggest that elevated nitric oxide production could be important in the pathogenesis of autoimmunity, and that treatments to block the production of Nitric oxide or block its effects might be valuable therapeutically.
Journal ArticleDOI
Cell nucleus and DNA fragmentation are not required for apoptosis
TL;DR: It is shown that cells enucleated with cytochalasin B still undergo apoptosis induced either by treatment with menadione, an oxidant quinone compound, or by triggering APO-1/Fas, a cell surface molecule involved in physiological cell death.
Journal ArticleDOI
Mature T cells of autoimmune lpr/lpr mice have a defect in antigen-stimulated suicide.
TL;DR: It is shown that Mutant lpr/lpr mice exhibit an autoimmune syndrome similar to systemic lupus erythematosus and a defect in antigen-stimulated suicide of activated T cells in mature CD4+ and CD8+ T cell compartments, suggesting that antigen- Stimulated death of mature cells may be important both in establishing peripheral tolerance and in limiting inflammation during normal immune responses.