Antigen-specific tolerance strategies for the prevention and treatment of autoimmune disease
暂无分享,去创建一个
[1] I. Cohen,et al. Treatment of new‐onset type 1 diabetes with peptide DiaPep277® is safe and associated with preserved beta‐cell function: extension of a randomized, double‐blind, phase II trial , 2007, Diabetes/metabolism research and reviews.
[2] M. Peakman,et al. Translational Mini‐Review Series on Type 1 Diabetes: Immune‐based therapeutic approaches for type 1 diabetes , 2007, Clinical and experimental immunology.
[3] F. Lublin,et al. Reactivation of JC virus and development of PML in patients with multiple sclerosis , 2007, Neurology.
[4] M. Rovaris,et al. Randomized, double-blind, dose-comparison study of glatiramer acetate in relapsing–remitting MS , 2007, Neurology.
[5] S. Miller,et al. Peripheral Tolerance Induction Using Ethylenecarbodiimide-Fixed APCs Uses both Direct and Indirect Mechanisms of Antigen Presentation for Prevention of Experimental Autoimmune Encephalomyelitis1 , 2007, The Journal of Immunology.
[6] S. Miller,et al. CNS myeloid DCs presenting endogenous myelin peptides 'preferentially' polarize CD4+ TH-17 cells in relapsing EAE , 2007, Nature Immunology.
[7] S. Miller,et al. Multi-peptide coupled-cell tolerance ameliorates ongoing relapsing EAE associated with multiple pathogenic autoreactivities. , 2006, Journal of autoimmunity.
[8] J. Bluestone,et al. Insulin-induced remission in new-onset NOD mice is maintained by the PD-1–PD-L1 pathway , 2006, The Journal of experimental medicine.
[9] J. Stroud,et al. FOXP3 Controls Regulatory T Cell Function through Cooperation with NFAT , 2006, Cell.
[10] H. Weiner,et al. Oral Tolerance: Therapeutic Implications for Autoimmune Diseases , 2006, Clinical & developmental immunology.
[11] R. Maki,et al. Immunomodulation in Type 1 Diabetes by NBI‐6024, an Altered Peptide Ligand of the Insulin B(9−23) Epitope , 2006, Scandinavian journal of immunology.
[12] C. Mathews,et al. DNA vaccination with an insulin construct and a chimeric protein binding to both CTLA4 and CD40 ameliorates type 1 diabetes in NOD mice , 2005, Gene Therapy.
[13] C. Guttmann,et al. A highly immunogenic trivalent T cell receptor peptide vaccine for multiple sclerosis , 2005, Multiple sclerosis.
[14] J. Strominger,et al. Differential induction of IgE-mediated anaphylaxis after soluble vs. cell-bound tolerogenic peptide therapy of autoimmune encephalomyelitis. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[15] P. Raskin,et al. Use of inhaled insulin in a basal/bolus insulin regimen in type 1 diabetic subjects: a 6-month, randomized, comparative trial. , 2005, Diabetes care.
[16] Michel Goldman,et al. Insulin needs after CD3-antibody therapy in new-onset type 1 diabetes. , 2005, The New England journal of medicine.
[17] J. Krischer,et al. Effects of oral insulin in relatives of patients with type 1 diabetes: The Diabetes Prevention Trial--Type 1. , 2005, Diabetes care.
[18] J. Bluestone,et al. Treatment with Nonmitogenic Anti-CD3 Monoclonal Antibody Induces CD4+ T Cell Unresponsiveness and Functional Reversal of Established Experimental Autoimmune Encephalomyelitis1 , 2005, The Journal of Immunology.
[19] S. Miller,et al. Epitope spreading initiates in the CNS in two mouse models of multiple sclerosis , 2005, Nature Medicine.
[20] Derin B Keskin,et al. Peptide 15-mers of defined sequence that substitute for random amino acid copolymers in amelioration of experimental autoimmune encephalomyelitis. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[21] H. Weiner. Current Issues in the Treatment of Human Diseases by Mucosal Tolerance , 2004, Annals of the New York Academy of Sciences.
[22] P. Raskin,et al. Oral Insulin Therapy to Prevent Progression of Immune‐Mediated (Type 1) Diabetes , 2004, Annals of the New York Academy of Sciences.
[23] F. Chirdo,et al. Oral Tolerance: Overview and Historical Perspectives , 2004, Annals of the New York Academy of Sciences.
[24] P. Pozzilli,et al. Cytokine profile and insulin antibody IgG subclasses in patients with recent onset Type 1 diabetes treated with oral insulin , 2004, Diabetologia.
[25] E. Liu. Peptide-specific amelioration of T cell-mediated pathogenesis in murine type 1 diabetes. , 2004, Clinical immunology.
[26] C. Brosnan,et al. Modified amino acid copolymers suppress myelin basic protein 85-99-induced encephalomyelitis in humanized mice through different effects on T cells. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[27] J. Penninger,et al. Essential role of the E3 ubiquitin ligase Cbl-b in T cell anergy induction. , 2004, Immunity.
[28] A. Rao,et al. E3 Ligases in T Cell Anergy—Turning Immune Responses into Tolerance , 2004, Science's STKE.
[29] E. Ranheim,et al. The Gene Related to Anergy in Lymphocytes, an E3 Ubiquitin Ligase, Is Necessary for Anergy Induction in CD4 T Cells1 , 2004, The Journal of Immunology.
[30] L. Mayer,et al. Therapeutic potential of oral tolerance , 2004, Nature Reviews Immunology.
[31] C. Berry,et al. Epitope-specific immunotherapy induces immune deviation of proinflammatory T cells in rheumatoid arthritis , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[32] R. Simon,et al. Expansion and Functional Relevance of High-Avidity Myelin-Specific CD4+ T Cells in Multiple Sclerosis , 2004, The Journal of Immunology.
[33] I. Messaoudi,et al. The many important facets of T-cell repertoire diversity , 2004, Nature Reviews Immunology.
[34] Bhagirath Singh,et al. CD4+CD25+ regulatory T cells generated in response to insulin B:9-23 peptide prevent adoptive transfer of diabetes by diabetogenic T cells. , 2003, Journal of autoimmunity.
[35] J. Bluestone,et al. TGF-β-dependent mechanisms mediate restoration of self-tolerance induced by antibodies to CD3 in overt autoimmune diabetes , 2003, Nature Medicine.
[36] J. Shabanowitz,et al. Identification of the β cell antigen targeted by a prevalent population of pathogenic CD8+ T cells in autoimmune diabetes , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[37] C. Fathman,et al. GRAIL: an E3 ubiquitin ligase that inhibits cytokine gene transcription is expressed in anergic CD4+ T cells. , 2003, Immunity.
[38] A. Norment,et al. Mucosal CD8α+ DC, with a plasmacytoid phenotype, induce differentiation and support function of T cells with regulatory properties , 2003, Immunology.
[39] J. Bluestone,et al. Activation of human T cells by FcR nonbinding anti-CD3 mAb, hOKT3γ1(Ala-Ala) , 2003 .
[40] L. Chatenoud. CD3-specific antibody-induced active tolerance: from bench to bedside , 2003, Nature reviews. Immunology.
[41] David H. Miller,et al. A controlled trial of natalizumab for relapsing multiple sclerosis. , 2003, The New England journal of medicine.
[42] J. Killestein. Anti-CD3 monoclonal antibody in new-onset type 1 diabetes mellitus. , 2002, The New England journal of medicine.
[43] J. Bluestone,et al. Modified anti-CD3 therapy in psoriatic arthritis: a phase I/II clinical trial. , 2002, The Journal of rheumatology.
[44] C. Arias,et al. Characterization of a new subpopulation of mouse CD8alpha+ B220+ dendritic cells endowed with type 1 interferon production capacity and tolerogenic potential. , 2002, Blood.
[45] Pamela S. Ohashi,et al. T-cell signalling and autoimmunity: molecular mechanisms of disease , 2002, Nature Reviews Immunology.
[46] Nitin J. Karandikar,et al. The role of CTLA‐4 in induction and maintenance of peripheral T cell tolerance , 2002, European journal of immunology.
[47] C. Mathieu,et al. A View on Beta Cell Transplantation in Diabetes , 2002, Annals of the New York Academy of Sciences.
[48] H. Weiner,et al. Oral tolerance to copolymer 1 in myelin basic protein (MBP) TCR transgenic mice: cross-reactivity with MBP-specific TCR and differential induction of anti-inflammatory cytokines. , 2002, International immunology.
[49] I. Cohen,et al. β-cell function in new-onset type 1 diabetes and immunomodulation with a heat-shock protein peptide (DiaPep277): a randomised, double-blind, phase II trial , 2001, The Lancet.
[50] K. Garcia,et al. Immunomodulation of Experimental Autoimmune Encephalomyelitis with Ordered Peptides Based on MHC-TCR Binding Motifs1 , 2001, The Journal of Immunology.
[51] R. Tisch,et al. Plasmid DNAs Encoding Insulin and Glutamic Acid Decarboxylase 65 Have Distinct Effects on the Progression of Autoimmune Diabetes in Nonobese Diabetic Mice1 , 2001, The Journal of Immunology.
[52] H. Weiner,et al. Mucosal administration of IL-10 enhances oral tolerance in autoimmune encephalomyelitis and diabetes. , 2001, International immunology.
[53] A. Rao,et al. Partners in transcription: NFAT and AP-1 , 2001, Oncogene.
[54] R. Pedotti,et al. An unexpected version of horror autotoxicus: anaphylactic shock to a self-peptide , 2001, Nature Immunology.
[55] A. Evans,et al. Induction of a non-encephalitogenic type 2 T helper-cell autoimmune response in multiple sclerosis after administration of an altered peptide ligand in a placebo-controlled, randomized phase II trial , 2000, Nature Medicine.
[56] J. Frank,et al. Encephalitogenic potential of the myelin basic protein peptide (amino acids 83–99) in multiple sclerosis: Results of a phase II clinical trial with an altered peptide ligand , 2000, Nature Medicine.
[57] C. Boitard,et al. Oral insulin administration and residual (β-cell function in recent-onset type 1 diabetes: a multicentre randomised controlled trial , 2000, The Lancet.
[58] A. T. N. Group,et al. No effect of oral insulin on residual beta-cell function in recent-onset Type I diabetes (the IMDIAB VII) , 2000, Diabetologia.
[59] V. Kuchroo,et al. IL-4, IL-10, IL-13, and TGF-β from an Altered Peptide Ligand-Specific Th2 Cell Clone Down-Regulate Adoptive Transfer of Experimental Autoimmune Encephalomyelitis , 2000, The Journal of Immunology.
[60] J. Bluestone,et al. Pathologic Role and Temporal Appearance of Newly Emerging Autoepitopes in Relapsing Experimental Autoimmune Encephalomyelitis1 , 2000, The Journal of Immunology.
[61] C. Boitard,et al. Oral insulin administration and residual beta-cell function in recent-onset type 1 diabetes: a multicentre randomised controlled trial. Diabète Insuline Orale group. , 2000, Lancet.
[62] D. Bourdette,et al. Differential susceptibility of human T(h)1 versus T(h) 2 cells to induction of anergy and apoptosis by ECDI/antigen-coupled antigen-presenting cells. , 2000, International immunology.
[63] M. V. von Herrath,et al. DNA immunization to prevent autoimmune diabetes. , 1999, The Journal of clinical investigation.
[64] A. Cross,et al. Oral administration of myelin basic protein is superior to myelin in suppressing established relapsing experimental autoimmune encephalomyelitis. , 1999, Journal of immunology.
[65] M. Sela,et al. Copolymer 1 acts against the immunodominant epitope 82-100 of myelin basic protein by T cell receptor antagonism in addition to major histocompatibility complex blocking. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[66] H. Weiner,et al. Oral tolerance: mechanisms and therapeutic applications. , 1999, Advances in immunology.
[67] M. Naramura,et al. Altered thymic positive selection and intracellular signals in Cbl-deficient mice. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[68] J. Kremer,et al. Treatment of rheumatoid arthritis with oral type II collagen. Results of a multicenter, double-blind, placebo-controlled trial. , 1998, Arthritis and rheumatism.
[69] Liu,et al. Complexities of applying nasal tolerance induction as a therapy for ongoing relapsing experimental autoimmune encephalomyelitis (EAE) in DA rats , 1998, Clinical and Experimental Immunology.
[70] F. Shi,et al. Nasal administration of myelin basic protein prevents relapsing experimental autoimmune encephalomyelitis in DA rats by activating regulatory cells expressing IL-4 and TGF-β mRNA , 1997, Journal of Neuroimmunology.
[71] K. Wucherpfennig,et al. Tolerance induction to myelin basic protein by intravenous synthetic peptides containing epitope P85VVHFFKNIVTP96 in chronic progressive multiple sclerosis , 1997, Journal of the Neurological Sciences.
[72] A. Sette,et al. A T cell receptor antagonist peptide induces T cells that mediate bystander suppression and prevent autoimmune encephalomyelitis induced with multiple myelin antigens. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[73] S. Miller,et al. Induction of antigen-specific tolerance for the treatment of ongoing, relapsing autoimmune encephalomyelitis: a comparison between oral and peripheral tolerance. , 1997, Journal of immunology.
[74] L. Nicholson,et al. T cell recognition of self and altered self antigens. , 1997, Critical reviews in immunology.
[75] S. Hauser,et al. Late Complications of Immune Deviation Therapy in a Nonhuman Primate , 1996, Science.
[76] S. Miller,et al. Epitope spreading , 1996, Current Opinion in Immunology.
[77] C. Whitacre,et al. Suppression of murine chronic relapsing experimental autoimmune encephalomyelitis by the oral administration of myelin basic protein. , 1996, Journal of immunology.
[78] S. Miller,et al. Inhibition of relapsing experimental autoimmune encephalomyelitis in SJL mice by feeding the immunodominant PLP139‐151 peptide , 1996, Journal of neuroscience research.
[79] A. Vandenbark,et al. Prevention and treatment of relapsing autoimmune encephalomyelitis with myelin peptide‐coupled splenocytes , 1996, Journal of neuroscience research.
[80] C. Whitacre,et al. Oral Tolerance in Experimental Autoimmune Encephalomyelitis , 1996, Annals of the New York Academy of Sciences.
[81] H. McFarland,et al. Intravenous antigen adrmnistration as a therapy for autoimmune demyelinating disease , 1996, Annals of neurology.
[82] Nitin J. Karandikar,et al. Blockade of CD28/B7-1 interaction prevents epitope spreading and clinical relapses of murine EAE. , 1995, Immunity.
[83] R. Strieter,et al. An important role for the chemokine macrophage inflammatory protein-1 alpha in the pathogenesis of the T cell-mediated autoimmune disease, experimental autoimmune encephalomyelitis. , 1995, Journal of immunology.
[84] V. Kuchroo,et al. An altered peptide ligand mediates immune deviation and prevents autoimmune encephalomyelitis. , 1995, Immunity.
[85] M. Samson,et al. Reversal of acute experimental autoimmune encephalomyelitis and prevention of relapses by treatment with a myelin basic protein peptide analogue modified to form long-lived peptide-MHC complexes. , 1995, Journal of immunology.
[86] J. W. Rose,et al. Copolymer 1 reduces relapse rate and improves disability in relapsing‐remitting multiple sclerosis , 1995, Neurology.
[87] S. Miller,et al. Functional evidence for epitope spreading in the relapsing pathology of experimental autoimmune encephalomyelitis , 1995, The Journal of experimental medicine.
[88] S. Miller,et al. Evolution of the T‐Cell Repertoire during the Course of Experimental Immune‐Mediated Demyelinating Diseases , 1995, Immunological reviews.
[89] Jeffrey A. Cohen,et al. Copolymer 1 reduces relapse rate and improves disability in relapsing-remitting multiple sclerosis: results of a phase III multicenter, double-blind placebo-controlled trial. The Copolymer 1 Multiple Sclerosis Study Group. , 1995, Neurology.
[90] D. Mitchell,et al. Reversal of experimental autoimmune encephalomyelitis by a soluble peptide variant of a myelin basic protein epitope: T cell receptor antagonism and reduction of interferon gamma and tumor necrosis factor alpha production , 1994, The Journal of experimental medicine.
[91] H. Weiner,et al. Regulatory T cell clones induced by oral tolerance: suppression of autoimmune encephalomyelitis. , 1994, Science.
[92] S. Miller,et al. The immunopathogenesis and regulation of T-cell-mediated demyelinating diseases. , 1994, Immunology today.
[93] H. Weiner,et al. Induction of anergy or active suppression following oral tolerance is determined by antigen dosage. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[94] J. Goverman,et al. T cell deletion in high antigen dose therapy of autoimmune encephalomyelitis. , 1994, Science.
[95] L. Chatenoud,et al. Anti-CD3 antibody induces long-term remission of overt autoimmunity in nonobese diabetic mice. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[96] E. Amento,et al. Induction of peripheral tolerance with peptide-specific anergy in experimental autoimmune neuritis. , 1993, Cellular immunology.
[97] D. Wraith,et al. Inhibition of experimental autoimmune encephalomyelitis by inhalation but not oral administration of the encephalitogenic peptide: influence of MHC binding affinity. , 1993, International immunology.
[98] H. Weiner,et al. Double-blind pilot trial of oral tolerization with myelin antigens in multiple sclerosis. , 1993, Science.
[99] A. Gaur,et al. Amelioration of autoimmune encephalomyelitis by myelin basic protein synthetic peptide-induced anergy. , 1992, Science.
[100] H. Weiner,et al. Oral tolerance to myelin basic protein and natural recovery from experimental autoimmune encephalomyelitis are associated with downregulation of inflammatory cytokines and differential upregulation of transforming growth factor beta, interleukin 4, and prostaglandin E expression in the brain , 1992, The Journal of experimental medicine.
[101] E. Sercarz,et al. Spreading of T-cell autoimmunity to cryptic determinants of an autoantigen , 1992, Nature.
[102] H. Burstein,et al. Aqueous antigens induce in vivo tolerance selectively in IL-2- and IFN-gamma-producing (Th1) cells. , 1992, Journal of immunology.
[103] S. Miller,et al. Regulation of the effector stages of experimental autoimmune encephalomyelitis via neuroantigen-specific tolerance induction. II. Fine specificity of effector T cell inhibition. , 1992, Journal of immunology.
[104] S. Miller,et al. Antigen-specific inhibition of the adoptive transfer of experimental autoimmune enceophalomyelitis in Lewis rats , 1992, Journal of Neuroimmunology.
[105] F. Sánchez‐Madrid,et al. Prevention of experimental autoimmune encephalomyelitis by antibodies against α4βl integrin , 1992, Nature.
[106] L. Donoso,et al. Inhibition of experimental autoimmune uveitis by retinal photoreceptor antigens coupled to spleen cells. , 1992, Cellular immunology.
[107] M. Sporn,et al. Suppressor T cells generated by oral tolerization to myelin basic protein suppress both in vitro and in vivo immune responses by the release of transforming growth factor beta after antigen-specific triggering. , 1992, Proceedings of the National Academy of Sciences of the United States of America.
[108] W. Karpus,et al. Antigen-specific tolerance as a therapy for experimental autoimmune encephalomyelitis. , 1992, International reviews of immunology.
[109] S. Sriram,et al. Treatment of chronic relapsing experimental allergic encephalomyelitis with the intravenous administration of splenocytes coupled to encephalitogenic peptide 91–103 of myelin basic protein , 1991, Journal of Neuroimmunology.
[110] C. Orosz,et al. Oral tolerance in experimental autoimmune encephalomyelitis. III. Evidence for clonal anergy. , 1991, Journal of immunology.
[111] S. Miller,et al. Successful treatment of paralytic relapses in adoptive experimental autoimmune encephalomyelitis via neuroantigen-specific tolerance. , 1991, Journal of immunology.
[112] R. Clark,et al. An antibody to lymphotoxin and tumor necrosis factor prevents transfer of experimental allergic encephalomyelitis , 1990, The Journal of experimental medicine.
[113] S. Miller,et al. Regulation of the effector stages of experimental autoimmune encephalomyelitis via neuroantigen-specific tolerance induction. , 1990, Journal of immunology.
[114] V. Tuohy,et al. Inhibition of murine relapsing experimental autoimmune encephalomyelitis by immune tolerance to proteolipid protein and its encephalitogenic peptides. , 1990, Journal of immunology.
[115] Lawrence Steinman,et al. Antigen recognition in autoimmune encephalomyelitis and the potential for peptide-mediated immunotherapy , 1989, Cell.
[116] C. Whitacre,et al. Suppression of experimental autoimmune encephalomyelitis by the oral administration of myelin basic protein. , 1988, Cellular immunology.
[117] R. Schwartz,et al. Antigen presentation by chemically modified splenocytes induces antigen- specific T cell unresponsiveness in vitro and in vivo , 1987, The Journal of experimental medicine.
[118] L. Steinman,et al. Administration of myelin basic protein-coupled spleen cells prevents experimental allergic encephalitis. , 1983, Cellular immunology.
[119] H. Drummond,et al. Immunological responses to fed protein antigens in mice. I. Reversal of oral tolerance to ovalbumin by cyclophosphamide. , 1982, Immunology.
[120] G. Sharp,et al. Suppression of experimental autoimmune thyroiditis in guinea pigs by pretreatment with thyroglobulin-coupled spleen cells. , 1980, Cellular immunology.
[121] D. Katz,et al. Regulation of IgE antibody production by serum molecules. V. Evidence that coincidental sensitization and imbalance in the normal damping mechanism results in "allergic breakthrough". , 1979, Journal of immunology.
[122] S. Miller,et al. The induction of cell-mediated immunity and tolerance with protein antigens coupled to syngeneic lymphoid cells , 1979, The Journal of experimental medicine.
[123] D. Katz,et al. Regulation of IgE antibody production by serum molecules. I. Serum from complete Freund's adjuvant-immune donors suppresses irradiation-enhanced IgE production in low responder mouse strains. , 1978, Journal of immunology.
[124] W. L. Benedict,et al. Multiple Sclerosis , 2007, Journal - Michigan State Medical Society.