Serum CD95 of relapsing remitting multiple sclerosis patients protects from CD95-mediated apoptosis

[1]  J. Dichgans,et al.  Increased serum levels of soluble CD95 (APO‐1/Fas) in relapsing‐remitting multiple sclerosis , 1998, Annals of neurology.

[2]  J. Tschopp,et al.  Myelin oligodendrocyte glycoprotein‐induced autoimmune encephalomyelitis is chronic/relapsing in perforin knockout mice, but monophasic in Fas‐ and Fas ligand‐deficient lpr and gld mice , 1997, European journal of immunology.

[3]  A. Cross,et al.  Fas and Fas ligand enhance the pathogenesis of experimental allergic encephalomyelitis, but are not essential for immune privilege in the central nervous system. , 1997, Journal of immunology.

[4]  V. Kuchroo,et al.  Fas- and FasL-deficient mice are resistant to induction of autoimmune encephalomyelitis. , 1997, Journal of immunology.

[5]  J. Dichgans,et al.  Human autoreactive and foreign antigen-specific T cells resist apoptosis induced by soluble recombinant CD95 ligand. , 1997, Journal of immunology.

[6]  J. Menonna,et al.  Cell death and birth in multiple sclerosis brain , 1997, Journal of the Neurological Sciences.

[7]  C. Raine,et al.  Multiple sclerosis: Oligodendrocytes display cell death–related molecules in situ but do not undergo apoptosis , 1997, Annals of neurology.

[8]  N. Yanagisawa,et al.  Detection of the soluble form of the Fas molecule in patients with multiple sclerosis and human T-lymphotropic virus type I-associated myelopathy , 1997, Journal of Neuroimmunology.

[9]  L. Weiner,et al.  Defective post–thymic tolerance mechanisms during the chronic progressive stage of multiple sclerosis , 1996, Nature Medicine.

[10]  J. Antel,et al.  Multiple Sclerosis: Fas Signaling in Oligodendrocyte Cell Death , 1996, The Journal of experimental medicine.

[11]  J. Menonna,et al.  Involvement of the CD95 (APO-1/Fas) receptor/ligand system in multiple sclerosis brain , 1996, The Journal of experimental medicine.

[12]  G. Starace,et al.  An N-terminal domain shared by Fas/Apo-1 (CD95) soluble variants prevents cell death in vitro. , 1996, Journal of immunology.

[13]  A. Abbas,et al.  The roles of costimulation and Fas in T cell apoptosis and peripheral tolerance. , 1996, Immunity.

[14]  R. Testi,et al.  Fas/Apo-1 (CD95) receptor lacking the intracytoplasmic signaling domain protects tumor cells from Fas-mediated apoptosis. , 1996, Journal of immunology.

[15]  M. Weller,et al.  Fas/APO-1 gene transfer for human malignant glioma. , 1995, Cancer research.

[16]  G. Fiucci,et al.  Three functional soluble forms of the human apoptosis-inducing Fas molecule are produced by alternative splicing. , 1995, Journal of immunology.

[17]  P. Krammer,et al.  Identification of soluble APO-1 in supernatants of human B- and T-cell lines and increased serum levels in B- and T-cell leukemias. , 1995, Blood.

[18]  S. Ju,et al.  Fas(CD95)/FasL interactions required for programmed cell death after T-cell activation , 1995, Nature.

[19]  Seamus J. Martin,et al.  Cell-autonomous Fas (CD95)/Fas-ligand interaction mediates activation-induced apoptosis in T-cell hybridomas , 1995, Nature.

[20]  P. Krammer,et al.  Autocrine T-cell suicide mediated by APO-1/(Fas/CD95) , 1995, Nature.

[21]  C. Smith,et al.  Fas ligand mediates activation-induced cell death in human T lymphocytes , 1995, The Journal of experimental medicine.

[22]  B. Weinshenker,et al.  Meta‐analysis of clinical studies of the efficacy of plasma exchange in the treatment of chronic progressive multiple sclerosis , 1995, Journal of clinical apheresis.

[23]  M. Weller,et al.  Anti-Fas/APO-1 antibody-mediated apoptosis of cultured human glioma cells. Induction and modulation of sensitivity by cytokines. , 1994, The Journal of clinical investigation.

[24]  D. Constam,et al.  Transforming growth factor‐β2 induces apoptosis of murine T cell clones without down‐regulating bcl‐2 mRNA expression , 1994, European journal of immunology.

[25]  Matthew J. Brauer,et al.  Protection from Fas-mediated apoptosis by a soluble form of the Fas molecule. , 1994, Science.

[26]  J. Goverman,et al.  T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis. , 1994, Science.

[27]  H. Lassmann,et al.  Apoptosis of T lymphocytes in experimental autoimmune encephalomyelitis. Evidence for programmed cell death as a mechanism to control inflammation in the brain. , 1993, The American journal of pathology.

[28]  Moses Rodriguez,et al.  Plasmapheresis in acute episodes of fulminant CNS inflammatory demyelination , 1993, Neurology.

[29]  M. Pender,et al.  Apoptosis in the nervous system in experimental allergic encephalomyelitis , 1991, Journal of the Neurological Sciences.