Lawrence Steinman

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. ncbi request reprint Janus faces of amyloid proteins in neuroinflammation
    Lawrence Steinman
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA, USA
    J Clin Immunol 34:S61-3. 2014
  2. ncbi request reprint Development of therapies for autoimmune disease at Stanford: a tale of multiple shots and one goal
    Lawrence Steinman
    Departments of Pediatrics, Neurology and Neurological Sciences, Stanford University, Stanford, CA, USA
    Immunol Res 58:307-14. 2014
  3. pmc Peroxisome proliferator-activated receptor (PPAR)alpha expression in T cells mediates gender differences in development of T cell-mediated autoimmunity
    Shannon E Dunn
    Department of Neurology and Neurological Studies, and 2Department of Pathology, Stanford University Medical Center, Stanford, CA 94305, USA
    J Exp Med 204:321-30. 2007
  4. pmc The protective and therapeutic function of small heat shock proteins in neurological diseases
    Sara E Brownell
    Department of Neurology and Neurological Sciences, Stanford University Stanford, CA, USA
    Front Immunol 3:74. 2012
  5. doi request reprint Immunology of relapse and remission in multiple sclerosis
    Lawrence Steinman
    Departments of Pediatrics, Neurology and Neurological Sciences, Stanford University, Stanford, California 94305 email
    Annu Rev Immunol 32:257-81. 2014
  6. doi request reprint Piet Mondrian's trees and the evolution in understanding multiple sclerosis, Charcot Prize Lecture 2011
    Lawrence Steinman
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305, USA
    Mult Scler 19:5-14. 2013
  7. doi request reprint Inflammatory cytokines at the summits of pathological signal cascades in brain diseases
    Lawrence Steinman
    Departments of Pediatrics and Neurology and Neurological Sciences, Stanford University, Beckman Center for Molecular Medicine, Stanford, CA 94305 5316, USA
    Sci Signal 6:pe3. 2013
  8. pmc The discovery of natalizumab, a potent therapeutic for multiple sclerosis
    Lawrence Steinman
    Department of Pediatrics, Interdepartmental Program in Immunology, Stanford University, Stanford, CA 94305, USA
    J Cell Biol 199:413-6. 2012
  9. pmc Severe anaphylactic reactions to glutamic acid decarboxylase (GAD) self peptides in NOD mice that spontaneously develop autoimmune type 1 diabetes mellitus
    Rosetta Pedotti
    Department of Pathology, Stanford University School of Medicine, Stanford, California, USA
    BMC Immunol 4:2. 2003
  10. ncbi request reprint Elaborate interactions between the immune and nervous systems
    Lawrence Steinman
    Department of Neurological Sciences and Neurology and Pediatrics, Interdepartmental Program in Immunology, Beckman Center for Molecular Medicine, Stanford, California 94305, USA
    Nat Immunol 5:575-81. 2004

Research Grants

  1. IN VIVO TREATMENT OF EAE WITH ANTI I-A ANTIBODIES
    Lawrence Steinman; Fiscal Year: 1993
  2. Autoantibody Arrays Guide Tolergenic Therapy for Multiple Sclerosis
    Lawrence Steinman; Fiscal Year: 2010
  3. IN VIVO TREATMENT OF EAE WITH ANTI I-A ANTIBODIES
    Lawrence Steinman; Fiscal Year: 2000
  4. IN VIVO TREATMENT OF EAE WITH ANTI I-A ANTIBODIES
    Lawrence Steinman; Fiscal Year: 2000
  5. IN VIVO TREATMENT OF EAE WITH ANTI I-A ANTIBODIES
    Lawrence Steinman; Fiscal Year: 1999
  6. PEPTIDE MEDIATED IMMUNOTHERAPY FOR AUTOIMMUNE DISEASE
    Lawrence Steinman; Fiscal Year: 1993
  7. PEPTIDE MEDIATED IMMUNOTHERAPY FOR AUTOIMMUNE DISEASE
    Lawrence Steinman; Fiscal Year: 1992
  8. PEPTIDE MEDIATED IMMUNOTHERAPY FOR AUTOIMMUNE DISEASE
    Lawrence Steinman; Fiscal Year: 1991
  9. IN VIVO TREATMENT OF EAE WITH ANTI I-A ANTIBODIES
    Lawrence Steinman; Fiscal Year: 2001
  10. PEPTIDE MEDIATED IMMUNOTHERAPY FOR AUTOIMMUNE DISEASE
    Lawrence Steinman; Fiscal Year: 2001

Detail Information

Publications101 found, 100 shown here

  1. ncbi request reprint Janus faces of amyloid proteins in neuroinflammation
    Lawrence Steinman
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA, USA
    J Clin Immunol 34:S61-3. 2014
    ..These experiments indicate that amyloid forming molecules have Janus faces, providing unexpected benefit for neuroinflammatory conditions. ..
  2. ncbi request reprint Development of therapies for autoimmune disease at Stanford: a tale of multiple shots and one goal
    Lawrence Steinman
    Departments of Pediatrics, Neurology and Neurological Sciences, Stanford University, Stanford, CA, USA
    Immunol Res 58:307-14. 2014
    ..The milieu within Stanford Immunology has helped to nurture these efforts to translate discoveries in immunology and to take them from bench to bedside...
  3. pmc Peroxisome proliferator-activated receptor (PPAR)alpha expression in T cells mediates gender differences in development of T cell-mediated autoimmunity
    Shannon E Dunn
    Department of Neurology and Neurological Studies, and 2Department of Pathology, Stanford University Medical Center, Stanford, CA 94305, USA
    J Exp Med 204:321-30. 2007
    ..These results suggest that males are less prone to develop Th1-mediated autoimmunity because they have higher T cell expression of PPARalpha...
  4. pmc The protective and therapeutic function of small heat shock proteins in neurological diseases
    Sara E Brownell
    Department of Neurology and Neurological Sciences, Stanford University Stanford, CA, USA
    Front Immunol 3:74. 2012
    ..Furthermore, it focuses on recent studies that have investigated the therapeutic potential of sHSPs for neurological diseases. Finally, it will explain what we think is the function of endogenous sHSPs in neurological diseases...
  5. doi request reprint Immunology of relapse and remission in multiple sclerosis
    Lawrence Steinman
    Departments of Pediatrics, Neurology and Neurological Sciences, Stanford University, Stanford, California 94305 email
    Annu Rev Immunol 32:257-81. 2014
    ..Despite substantial progress in controlling relapses with the current armamentarium of medications, there is much to learn and ever more effective and safe therapies to develop. ..
  6. doi request reprint Piet Mondrian's trees and the evolution in understanding multiple sclerosis, Charcot Prize Lecture 2011
    Lawrence Steinman
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305, USA
    Mult Scler 19:5-14. 2013
    ....
  7. doi request reprint Inflammatory cytokines at the summits of pathological signal cascades in brain diseases
    Lawrence Steinman
    Departments of Pediatrics and Neurology and Neurological Sciences, Stanford University, Beckman Center for Molecular Medicine, Stanford, CA 94305 5316, USA
    Sci Signal 6:pe3. 2013
    ..Targeting these cytokines or their receptors can alter the course of several neurological diseases, but the effects may be beneficial or harmful...
  8. pmc The discovery of natalizumab, a potent therapeutic for multiple sclerosis
    Lawrence Steinman
    Department of Pediatrics, Interdepartmental Program in Immunology, Stanford University, Stanford, CA 94305, USA
    J Cell Biol 199:413-6. 2012
    ..Was it sheer luck that these results led to the development of a drug for MS?..
  9. pmc Severe anaphylactic reactions to glutamic acid decarboxylase (GAD) self peptides in NOD mice that spontaneously develop autoimmune type 1 diabetes mellitus
    Rosetta Pedotti
    Department of Pathology, Stanford University School of Medicine, Stanford, California, USA
    BMC Immunol 4:2. 2003
    ....
  10. ncbi request reprint Elaborate interactions between the immune and nervous systems
    Lawrence Steinman
    Department of Neurological Sciences and Neurology and Pediatrics, Interdepartmental Program in Immunology, Beckman Center for Molecular Medicine, Stanford, California 94305, USA
    Nat Immunol 5:575-81. 2004
    ..Neurobiologists and immunologists are exploring common ideas like the synapse to understand properties such as memory that are shared in these two systems...
  11. pmc Nuanced roles of cytokines in three major human brain disorders
    Lawrence Steinman
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, USA
    J Clin Invest 118:3557-63. 2008
    ....
  12. ncbi request reprint Immune therapy for autoimmune diseases
    Lawrence Steinman
    Department of Neurological Sciences and Neurology, and Interdepartmental Program in Immunology, Stanford University, Stanford, CA 94305, USA
    Science 305:212-6. 2004
    ..In many organ-specific autoimmune diseases, the identity of the molecules attacked by T cells and autoantibodies is known and attempts are under way to tolerize the immune system with a high level of specificity to these targets...
  13. ncbi request reprint New targets for treatment of multiple sclerosis
    Lawrence Steinman
    Department of Neurology and Neurological Sciences, Interdepartmental Program in Immunology, Stanford University, Stanford CA 94305, United States
    J Neurol Sci 274:1-4. 2008
    ..These four proteins are critical in controlling relapse and remission in MS...
  14. pmc A rush to judgment on Th17
    Lawrence Steinman
    Department of Neurology and Neurological Sciences and the Interdepartmental Program in Immunology, Beckman Center for Molecular Medicine, Stanford University, Stanford, CA 94305, USA
    J Exp Med 205:1517-22. 2008
    ..Thus, the role of Th17 cytokines as the central mediators of pathological tissue damage seems to require clarification...
  15. ncbi request reprint Blocking adhesion molecules as therapy for multiple sclerosis: natalizumab
    Lawrence Steinman
    Stanford University, Stanford, California 94305, USA
    Nat Rev Drug Discov 4:510-8. 2005
    ....
  16. ncbi request reprint Virtues and pitfalls of EAE for the development of therapies for multiple sclerosis
    Lawrence Steinman
    Department of Neurology and Neurological Sciences, Chair Interdepartmental Program in Immunology, Stanford University, Stanford, CA 94305, USA
    Trends Immunol 26:565-71. 2005
    ..However, EAE has failed to predict the outcome of certain approaches. The reasons underlying such failures are discussed here...
  17. ncbi request reprint Antigen-specific therapy of multiple sclerosis: the long-sought magic bullet
    Lawrence Steinman
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305, USA
    Neurotherapeutics 4:661-5. 2007
    ....
  18. ncbi request reprint Suppression of autoimmunity via microbial mimics of altered peptide ligands
    L Steinman
    Dept of Neurological Sciences and Interdepartmental Program in Immunology, Beckman Center for Molecular Medicine B002, Stanford University School of Medicine, CA 94305, USA
    Curr Top Microbiol Immunol 296:55-63. 2005
    ..Autoimmunity could therefore be modulated via microbial immunity, which may account for relapse and remission of ongoing disease...
  19. ncbi request reprint Controlling autoimmunity in sporadic inclusion-body myositis
    Lawrence Steinman
    Department of Neurology and Neurological Sciences, Beckman Center for Molecular Medicine, Stanford University, Stanford, CA 94305, USA
    Neurology 66:S56-8. 2006
  20. ncbi request reprint How to successfully apply animal studies in experimental allergic encephalomyelitis to research on multiple sclerosis
    Lawrence Steinman
    Department of Neurology and Neurological Sciences, Stanford University, CA 94305, USA
    Ann Neurol 60:12-21. 2006
    ..There are pitfalls in overreliance on the EAE model, or on any animal model for any human disease. Nevertheless, over the past 73 years, the EAE model has proved itself remarkably useful for aiding research on MS...
  21. ncbi request reprint A brief history of T(H)17, the first major revision in the T(H)1/T(H)2 hypothesis of T cell-mediated tissue damage
    Lawrence Steinman
    Interdepartmental Program in Immunology, Department of Neurology and Neurological Sciences, Beckman Center for Molecular Medicine, Stanford University, Stanford, California 94305, USA
    Nat Med 13:139-45. 2007
    ..The evolution of our understanding of the T(H)17 pathway illuminates a shift in immunologists' perspectives regarding the basis of tissue damage, where for over 20 years the role of T(H)1 cells was considered paramount...
  22. ncbi request reprint State of the art. Four easy pieces: interconnections between tissue injury, intermediary metabolism, autoimmunity, and chronic degeneration
    Lawrence Steinman
    Interdepartmental Program in Immunology, Beckman Center for Molecular Medicine, Stanford University, CA 94305, USA
    Proc Am Thorac Soc 3:484-6. 2006
    ..Inflammatory, degenerative, and autoimmune neurological disease will be discussed in terms of their implications for pathogenic mechanisms underlying chronic obstructive pulmonary disease...
  23. ncbi request reprint A molecular trio in relapse and remission in multiple sclerosis
    Lawrence Steinman
    Department of Neurology and Neurological Sciences, Interdepartmental Program in Immunology, Beckman Center for Molecular Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
    Nat Rev Immunol 9:440-7. 2009
    ..This Review discusses how this molecular trio interacts to initiate relapses (in the case of osteopontin and alpha4beta1 integrin) and then to terminate them as remissions in multiple sclerosis (in the case of alphaB crystallin)...
  24. ncbi request reprint Shifting therapeutic attention in MS to osteopontin, type 1 and type 2 IFN
    Lawrence Steinman
    Department of Neurological Sciences, Beckman Center for Molecular Medicine, Stanford University, Stanford, CA 94305, USA
    Eur J Immunol 39:2358-60. 2009
    ..osteopontin and IL-17, are discussed in relation to the pathogenesis of MS. Osteopontin may be more important than Th1 or Th17 in the pathogenesis of RRMS. Trials targeting this small integrin-binding protein ought to be pursued in RRMS...
  25. ncbi request reprint Immunotherapy of multiple sclerosis: the end of the beginning
    L Steinman
    Beckman Center for Molecular Medicine, B002, Stanford University, Stanford, CA 94305, USA
    Curr Opin Immunol 13:597-600. 2001
    ..New directions for therapy of multiple sclerosis include blockade of alpha4 integrin, the use of altered peptide ligands, inhibition of Th1 cytokines, and DNA vaccination...
  26. ncbi request reprint Antigen specific immunotherapy of multiple sclerosis
    L Steinman
    Department of Neurological Science, Stanford University, California 94305, USA
    J Clin Immunol 21:93-8. 2001
    ..Induction of an antigen specific Th1-to-Th2 shift could achieve this aim, once side effects, such as allergic responses, are minimized with optimal dosing...
  27. ncbi request reprint Multiple sclerosis: deeper understanding of its pathogenesis reveals new targets for therapy
    Lawrence Steinman
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, California 94305, USA
    Annu Rev Neurosci 25:491-505. 2002
    ..Some of these participants may be useful targets for therapy...
  28. pmc The intricate interplay among body weight, stress, and the immune response to friend or foe
    Lawrence Steinman
    Interdepartmental Program in Immunology and Department of Neurological Sciences, Stanford University, Stanford, California 94205, USA
    J Clin Invest 111:183-5. 2003
  29. doi request reprint Inverse vaccination, the opposite of Jenner's concept, for therapy of autoimmunity
    L Steinman
    Department of Neurology and Neurological Science, Interdepartmental Program in Immunology, Stanford University, Stanford, CA94305, USA
    J Intern Med 267:441-51. 2010
    ..The method of specifically reducing a pathological adaptive autoimmune response is termed inverse vaccination...
  30. pmc Optic neuritis, a new variant of experimental encephalomyelitis, a durable model for all seasons, now in its seventieth year
    Lawrence Steinman
    Department of Neurology and Neurological Sciences, Stanford University Medical Center, Beckman Center B002, Stanford, CA 94305 5429, USA
    J Exp Med 197:1065-71. 2003
  31. ncbi request reprint Transcriptional analysis of targets in multiple sclerosis
    Lawrence Steinman
    Beckman Center for Molecular Medicine B002, Stanford University, Stanford, California 94305, USA
    Nat Rev Immunol 3:483-92. 2003
    ..This review focuses on multiple sclerosis and on the approaches that are being used to identify new targets that might be manipulated to control this disease...
  32. doi request reprint Mixed results with modulation of TH-17 cells in human autoimmune diseases
    Lawrence Steinman
    Department of Neurological Sciences and Interdepartmental Program in Immunology, Beckman Center for Molecular Medicine, Stanford University School of Medicine, Stanford, California, USA
    Nat Immunol 11:41-4. 2010
    ..Thus far, these outcomes in human trials have been mixed, with notable success in psoriasis and Crohn's disease but a negative result in relapsing-remitting multiple sclerosis...
  33. pmc Peroxisome proliferator-activated receptor delta limits the expansion of pathogenic Th cells during central nervous system autoimmunity
    Shannon E Dunn
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305, USA
    J Exp Med 207:1599-608. 2010
    ..Collectively, these findings suggest that PPAR-delta serves as an important molecular brake for the control of autoimmune inflammation...
  34. ncbi request reprint Treatment of autoimmune neuroinflammation with a synthetic tryptophan metabolite
    Michael Platten
    Department of Neurology and Neurological Sciences, Beckman Center for Molecular Medicine, Stanford University, Stanford, CA 94305, USA
    Science 310:850-5. 2005
    ..Trp catabolites and their derivatives offer a new strategy for treating T(H)1-mediated autoimmune diseases such as MS...
  35. ncbi request reprint An immunomodulatory GpG oligonucleotide for the treatment of autoimmunity via the innate and adaptive immune systems
    Peggy P Ho
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Beckman Center for Molecular Medicine, Stanford, CA 94305 5316, USA
    J Immunol 171:4920-6. 2003
    ..Moreover, this immunomodulatory GpG ODN suppresses the severity of experimental autoimmune encephalomyelitis in mice, a prototypic Th1-mediated animal disease model for multiple sclerosis...
  36. ncbi request reprint Tolerizing DNA vaccines for autoimmune arthritis
    Peggy P Ho
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    Autoimmunity 39:675-82. 2006
    ....
  37. ncbi request reprint Immunity to the extracellular domain of Nogo-A modulates experimental autoimmune encephalomyelitis
    Paulo Fontoura
    Department of Neurology and Neurological Sciences, School of Medicine, Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA
    J Immunol 173:6981-92. 2004
    ..These results indicate that some T cell and B cell immune responses to Nogo-66 are associated with suppression of ongoing EAE, whereas other Nogo-66 epitopes can be encephalitogenic...
  38. ncbi request reprint A suppressive oligodeoxynucleotide enhances the efficacy of myelin cocktail/IL-4-tolerizing DNA vaccination and treats autoimmune disease
    Peggy P Ho
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, CA 94305, USA
    J Immunol 175:6226-34. 2005
    ..These results demonstrate that suppressive GpG-ODN is a simple and highly effective novel therapeutic adjuvant that will boost the efficacy of Ag-specific tolerizing DNA vaccines used for treating Th1-mediated autoimmune diseases...
  39. pmc Immunomodulatory synergy by combination of atorvastatin and glatiramer acetate in treatment of CNS autoimmunity
    Olaf Stuve
    Department of Neurology and Program in Immunology, University of California, San Francisco, San Francisco, California, USA
    J Clin Invest 116:1037-44. 2006
    ..Our results demonstrate that agents with different mechanisms of immune modulation can combine in a synergistic manner for the treatment of CNS autoimmunity and provide rationale for testing the combination of atorvastatin and GA in MS...
  40. pmc Epitope spreading to citrullinated antigens in mouse models of autoimmune arthritis and demyelination
    Brian A Kidd
    Department of Medicine, Division of Immunology and Rheumatology, CCSR 4135, 269 Campus Dr, Stanford University School of Medicine, Stanford, CA, USA
    Arthritis Res Ther 10:R119. 2008
    ..Citrullination is the post-translational conversion of arginine to citrulline by peptidyl arginine deiminase, and increased citrullination of proteins is observed in the joint tissue in RA and in brain tissue in multiple sclerosis (MS)...
  41. pmc Inhibitory role for GABA in autoimmune inflammation
    Roopa Bhat
    Department of Neurology and Neurological Sciences, Beckman Center for Molecular Medicine, Stanford University, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 107:2580-5. 2010
    ..GABAergic agents act directly on APCs, decreasing MAPK signals and diminishing subsequent adaptive inflammatory responses to myelin proteins...
  42. pmc Inhibition of HMGcoA reductase by atorvastatin prevents and reverses MYC-induced lymphomagenesis
    Catherine M Shachaf
    Division of Medical Oncology, Department of Medicine, Stanford University, Stanford, CA 94305 5151, USA
    Blood 110:2674-84. 2007
    ..Thus, atorvastatin, by inhibiting HMGcoA reductase, induces changes in phosphoprotein signaling that in turn prevent MYC-induced lymphomagenesis...
  43. pmc Glia-dependent TGF-beta signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis
    Jian Luo
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305 5235, USA
    J Clin Invest 117:3306-15. 2007
    ..Importantly, inhibition of TGF-beta signaling may have benefits in the treatment of the acute phase of autoimmune CNS inflammation...
  44. pmc Janus-like opposing roles of CD47 in autoimmune brain inflammation in humans and mice
    May H Han
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Exp Med 209:1325-34. 2012
    ..Immune regulation and phagocytosis are mechanisms for CD47 signaling in autoimmune neuroinflammation. Depending on the cell type, location, and disease stage, CD47 has Janus-like roles, with opposing effects on EAE pathogenesis...
  45. ncbi request reprint Failure of oral atorvastatin to modulate a murine model of systemic lupus erythematosus
    Kareem L Graham
    Stanford University School of Medicine, Stanford, California 94305, USA
    Arthritis Rheum 58:2098-104. 2008
    ..In this study, we attempted to treat a widely studied murine model of spontaneous systemic lupus erythematosus (SLE) with atorvastatin...
  46. ncbi request reprint Treatment with a toll-like receptor inhibitory GpG oligonucleotide delays and attenuates lupus nephritis in NZB/W mice
    Kareem L Graham
    Department of Medicine, Stanford University School of Medicine, CA 94305, USA
    Autoimmunity 43:140-55. 2010
    ....
  47. pmc PPAR-delta senses and orchestrates clearance of apoptotic cells to promote tolerance
    Lata Mukundan
    Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA
    Nat Med 15:1266-72. 2009
    ..Thus, PPAR-delta has a pivotal role in orchestrating the timely disposal of apoptotic cells by macrophages, ensuring that tolerance to self is maintained...
  48. pmc Autoimmunity against fibrinogen mediates inflammatory arthritis in mice
    Peggy P Ho
    Department of Neurological and Neurologic Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Immunol 184:379-90. 2010
    ..These observations demonstrate that fibrinogen is arthritogenic in mice and that the pathogenesis of FIA is mediated by both autoantibodies and fibrinogen-reactive T cells...
  49. pmc Multiple elements of the allergic arm of the immune response modulate autoimmune demyelination
    Rosetta Pedotti
    Department of Neurology and Neurological Science, Stanford University Medical Center, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 100:1867-72. 2003
    ..The pathogenesis of demyelination must now be viewed as encompassing elements of both Th1 responses and "allergic" responses...
  50. pmc Th17 cells induce Th1-polarizing monocyte-derived dendritic cells
    Matthew G Davidson
    Department of Pathology, Blood Center, Stanford University School of Medicine, Palo Alto, CA 94304, USA
    J Immunol 191:1175-87. 2013
    ....
  51. doi request reprint Type 1 interferons cool the inflamed brain
    Robert C Axtell
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305, USA
    Immunity 28:600-2. 2008
    ..In this issue of Immunity, Prinz et al. (2008) elucidate an intriguing portrait of the pleiotropic effects of type 1 interferons in taming brain inflammation...
  52. pmc Tyrosine kinase inhibitors ameliorate autoimmune encephalomyelitis in a mouse model of multiple sclerosis
    Oliver Crespo
    Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Clin Immunol 31:1010-20. 2011
    ..Our findings suggest that GW2580 and the FDA-approved drugs imatinib and sorafenib have potential as novel therapeutics for the treatment of autoimmune demyelinating disease...
  53. ncbi request reprint Late pregnancy suppresses relapses in experimental autoimmune encephalomyelitis: evidence for a suppressive pregnancy-related serum factor
    Annette Langer-Gould
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Immunol 169:1084-91. 2002
    ..In conclusion, serum from late pregnancy has the capacity to down-regulate T cell responses and might be associated with the amelioration of disease activity in experimental autoimmune encephalomyelitis...
  54. ncbi request reprint Protective and therapeutic role for alphaB-crystallin in autoimmune demyelination
    Shalina S Ousman
    Department of Neurology and Neurological Sciences, Stanford University Stanford, California 94305, USA
    Nature 448:474-9. 2007
    ..Thus, the immune response against a negative regulator of inflammation, CRYAB, in multiple sclerosis, would exacerbate inflammation and demyelination. This can be countered by giving CRYAB itself for therapy of ongoing disease...
  55. pmc Amyloid fibrils composed of hexameric peptides attenuate neuroinflammation
    Michael P Kurnellas
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305 5316, USA
    Sci Transl Med 5:179ra42. 2013
    ..Amyloid fibrils thus may provide benefit in MS and other neuroinflammatory disorders...
  56. pmc Isoprenoids determine Th1/Th2 fate in pathogenic T cells, providing a mechanism of modulation of autoimmunity by atorvastatin
    Shannon E Dunn
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305, USA
    J Exp Med 203:401-12. 2006
    ..Thus, by connecting isoprenoid availability to regulation of Th1/Th2 fate, we have elucidated a mechanism by which AT may suppress Th1-mediated central nervous system autoimmune disease...
  57. pmc Reversal of paralysis and reduced inflammation from peripheral administration of β-amyloid in TH1 and TH17 versions of experimental autoimmune encephalomyelitis
    Jacqueline L Grant
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305, USA
    Sci Transl Med 4:145ra105. 2012
    ..Because Aβ42 and Aβ40 ameliorate experimental autoimmune inflammation targeting the CNS, we might now consider its potential anti-inflammatory role in other neuropathological conditions...
  58. pmc Angiotensin II sustains brain inflammation in mice via TGF-beta
    Tobias V Lanz
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, USA
    J Clin Invest 120:2782-94. 2010
    ..These data suggest that AT1R antagonists, frequently prescribed as antihypertensives, may be useful to interrupt this proinflammatory, CNS-specific pathway in individuals with MS...
  59. ncbi request reprint The HMG-CoA reductase inhibitor, atorvastatin, promotes a Th2 bias and reverses paralysis in central nervous system autoimmune disease
    Sawsan Youssef
    Department of Neurology and Neurological Sciences, Beckman Center for Molecular Medicine, Stanford University, Stanford, California 94305, USA
    Nature 420:78-84. 2002
    ..Thus, atorvastatin has pleiotropic immunomodulatory effects involving both APC and T-cell compartments. Statins may be beneficial for multiple sclerosis and other Th1-mediated autoimmune diseases...
  60. pmc T helper type 1 and 17 cells determine efficacy of interferon-beta in multiple sclerosis and experimental encephalomyelitis
    Robert C Axtell
    Department of Neurology and Neurological Sciences, Stanford University, Stanford, California, USA
    Nat Med 16:406-12. 2010
    ..Hence, IFN-beta is proinflammatory in T(H)17-induced EAE. Moreover, a high IL-17F concentration in the serum of people with RRMS is associated with nonresponsiveness to therapy with IFN-beta...
  61. ncbi request reprint Interferon-gamma-producing T cells, pregnancy, and postpartum relapses of multiple sclerosis
    Annette Langer-Gould
    Department of Health Research and Policy, School of Medicine, Stanford University, Stanford, CA 94305, USA
    Arch Neurol 67:51-7. 2010
    ..To determine whether fluctuations in functional T-cell subsets can explain why multiple sclerosis (MS) relapses decline during pregnancy and increase in the postpartum period...
  62. pmc Preemptive HMG-CoA reductase inhibition provides graft-versus-host disease protection by Th-2 polarization while sparing graft-versus-leukemia activity
    Robert Zeiser
    Division of Blood and Marrow Transplantation, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
    Blood 110:4588-98. 2007
    ....
  63. pmc Defective sphingosine 1-phosphate receptor 1 (S1P1) phosphorylation exacerbates TH17-mediated autoimmune neuroinflammation
    Christopher S Garris
    1 Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, USA 2 Graduate Program in Immunology, Division of Medical Sciences, Harvard Medical School, Boston, Massachusetts, USA 3
    Nat Immunol 14:1166-72. 2013
    ..S1P1 directly activated the Jak-STAT3 signal-transduction pathway via IL-6. Impaired S1P1 phosphorylation enhances TH17 polarization and exacerbates autoimmune neuroinflammation. These mechanisms may be pathogenic in MS. ..
  64. ncbi request reprint Proteomic analysis of active multiple sclerosis lesions reveals therapeutic targets
    May H Han
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA
    Nature 451:1076-81. 2008
    ..A proteomic approach illuminated potential therapeutic targets selective for specific pathological stages of MS and implicated participation of the coagulation cascade...
  65. pmc Selective tyrosine kinase inhibition by imatinib mesylate for the treatment of autoimmune arthritis
    Ricardo T Paniagua
    Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA
    J Clin Invest 116:2633-42. 2006
    ..Imatinib-mediated inhibition of a spectrum of signal transduction pathways and the downstream pathogenic cellular responses may provide a powerful approach to treat RA and other inflammatory diseases...
  66. ncbi request reprint Protein and peptide array analysis of autoimmune disease
    William H Robinson
    Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA
    Biotechniques . 2002
    ..Proteomic determination of autoantibody profiles can be utilized for diagnosis, prognostication, and guiding tolerizing therapy for autoimmune disease...
  67. ncbi request reprint Protein microarrays guide tolerizing DNA vaccine treatment of autoimmune encephalomyelitis
    William H Robinson
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
    Nat Biotechnol 21:1033-9. 2003
    ..Proteomic monitoring of autoantibody responses provides a useful approach to monitor autoimmune disease and to develop and tailor disease- and patient-specific tolerizing DNA vaccines...
  68. doi request reprint IL-17 contributes to the development of chronic rejection in a murine heart transplant model
    Satoshi Itoh
    Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Clin Immunol 30:235-40. 2010
    ..This study illustrates that IL-17 contributes to the pathogenesis of chronic allograft rejection...
  69. ncbi request reprint Osteopontin-induced relapse and progression of autoimmune brain disease through enhanced survival of activated T cells
    Eun Mi Hur
    Interdepartmental Program in Immunology, Stanford University School of Medicine, Stanford, California 94305, USA
    Nat Immunol 8:74-83. 2007
    ..Those mechanisms collectively suppressed the death of myelin-reactive T cells, linking Opn to the relapses and insidious progression characterizing multiple sclerosis...
  70. doi request reprint Interleukin-17 accelerates allograft rejection by suppressing regulatory T cell expansion
    Satoshi Itoh
    Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA
    Circulation 124:S187-96. 2011
    ..However, the precise role in allograft rejection remains uncertain. In the present study, we investigated the role of IL-17 in acute allograft rejection using IL-17-deficient mice...
  71. ncbi request reprint Millennium Award. Proteomics for the development of DNA tolerizing vaccines to treat autoimmune disease
    William H Robinson
    Department of Neurology, Stanford University School of Medicine, Stanford, California 94305, USA
    Clin Immunol 103:7-12. 2002
    ..Through integration of proteomics with specific tolerizing therapies, we are developing a comprehensive approach to treat human autoimmune disease...
  72. pmc Therapeutic effects of systemic administration of chaperone αB-crystallin associated with binding proinflammatory plasma proteins
    Jonathan B Rothbard
    Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, California 94305 5316, USA
    J Biol Chem 287:9708-21. 2012
    ....
  73. pmc Bioluminescence in vivo imaging of autoimmune encephalomyelitis predicts disease
    Jian Luo
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA
    J Neuroinflammation 5:6. 2008
    ..The disease is scored typically by observing signs of paralysis, which do not always correspond with pathological changes...
  74. ncbi request reprint Lipid microarrays identify key mediators of autoimmune brain inflammation
    Jennifer L Kanter
    Department of Microbiology and Immunology, Stanford University School of Medicine, 279 Campus Drive, Stanford, California 94305, USA
    Nat Med 12:138-43. 2006
    ..Thus, autoimmune responses to sulfatide and other lipids are present in individuals with multiple sclerosis and in EAE, and may contribute to the pathogenesis of autoimmune demyelination...
  75. pmc Autoantibody profiling for the study and treatment of autoimmune disease
    Wolfgang Hueber
    Department of Medicine, Division of Rheumatology and Immunology, Stanford University School of Medicine, California, USA
    Arthritis Res 4:290-5. 2002
    ..In the coming decades, proteomics technologies will broaden our understanding of the underlying mechanisms of and will further our ability to diagnose, prognosticate and treat autoimmune disease...
  76. pmc Microarray profiling of antibody responses against simian-human immunodeficiency virus: postchallenge convergence of reactivities independent of host histocompatibility type and vaccine regimen
    Henry E Neuman de Vegvar
    Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
    J Virol 77:11125-38. 2003
    ..These data suggest that the functional diversity of anti-SHIV B-cell responses is highly limited in the presence of persisting antigen...
  77. ncbi request reprint Protein arrays for autoantibody profiling and fine-specificity mapping
    William H Robinson
    Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA
    Proteomics 3:2077-84. 2003
    ..In addition to identifying autoantigens and mapping immunodominant epitopes, proteomic analysis of autoantibody responses will further enable diagnosis, prognosis, and tailoring of antigen-specific tolerizing therapy...
  78. pmc Thymic selection determines gammadelta T cell effector fate: antigen-naive cells make interleukin-17 and antigen-experienced cells make interferon gamma
    Kirk D C Jensen
    Department of Microbiology and Immunology, Stanford University, Stanford, CA 94305, USA
    Immunity 29:90-100. 2008
    ..The swift IL-17 response mounted by antigen-naive gammadelta T cells suggests a critical role for these cells at the onset of an acute inflammatory response to novel antigens...
  79. ncbi request reprint Immunomodulatory vaccination in autoimmune disease
    Irene Urbanek-Ruiz
    Department of Medicine, Division of Immunology, Center for Clinical Immunology at Stanford, Stanford University School of Medicine, 269 Campus Drive, Rm 2240, Stanford, CA 94305, USA
    Endocrinol Metab Clin North Am 31:441-56, viii-ix. 2002
    ....
  80. doi request reprint Socioeconomic trends in hospitalization for multiple sclerosis
    Shivanand P Lad
    Outcomes Research Laboratory, VA Palo Alto Health Care System, Palo Alto, CA 94304, USA
    Neuroepidemiology 35:93-9. 2010
    ..Little is known about the acute hospitalization costs and characteristics. We examined the trends in MS hospitalizations from 1993 to 2006...
  81. ncbi request reprint High-throughput methods for measuring autoantibodies in systemic lupus erythematosus and other autoimmune diseases
    Kareem L Graham
    Division of Immunology and Rheumatology, Department of Medicine, VA Palo Alto Health Care System, Palo Alto, CA 94304, USA
    Autoimmunity 37:269-72. 2004
    ..However, the next set of challenges is just right around the corner. As data and statistical analysis tools become more robust, it will be possible to generate and approach new hypotheses at an unprecedented pace...
  82. ncbi request reprint Photogenerated glycan arrays identify immunogenic sugar moieties of Bacillus anthracis exosporium
    Denong Wang
    Carbohydrate Microarray Laboratory, Stanford University School of Medicine, Stanford, CA, USA
    Proteomics 7:180-4. 2007
    ..anthracis exosporium. Since this sugar moiety is highly specific for the spores of B. anthracis, it appears to be a key biomarker for detection of B. anthracis spores and development of novel vaccines that target anthrax spores...
  83. ncbi request reprint Proteomics technologies for the study of autoimmune disease
    William H Robinson
    Stanford University School of Medicine, Stanford, California 94305, USA
    Arthritis Rheum 46:885-93. 2002
  84. ncbi request reprint Genomic and proteomic analysis of multiple sclerosis. Opinion
    William H Robinson
    Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA
    Curr Opin Immunol 15:660-7. 2003
    ....
  85. ncbi request reprint Autoantigen microarrays for multiplex characterization of autoantibody responses
    William H Robinson
    Division of Immunology and Rheumatology, Department of Medicine, Stanford, California, USA
    Nat Med 8:295-301. 2002
    ..Autoantigen microarrays represent a powerful tool to study the specificity and pathogenesis of autoantibody responses, and to identify and define relevant autoantigens in human autoimmune diseases...
  86. ncbi request reprint Gene-microarray analysis of multiple sclerosis lesions yields new targets validated in autoimmune encephalomyelitis
    Christopher Lock
    Department of Neurology and Neurological Sciences, Beckman Center, Stanford University, Stanford, California, USA
    Nat Med 8:500-8. 2002
    ..These results in EAE corroborate the microarray studies on MS lesions. Large-scale analysis of transcripts in MS lesions elucidates new aspects of pathology and opens possibilities for therapy...
  87. ncbi request reprint Progressive multifocal leukoencephalopathy and multiple sclerosis: lessons from natalizumab
    Annette Langer-Gould
    Stanford University School of Medicine, HRP Redwood Building, Room T202, MC 5405, Stanford, CA 94305, USA
    Curr Neurol Neurosci Rep 6:253-8. 2006
    ..Finally, we discuss what additional natalizumab efficacy data need to be presented before any decisions should be made about treating RRMS patients with a high risk of developing long-term disability...
  88. ncbi request reprint Induction of antigen-specific tolerance in multiple sclerosis after immunization with DNA encoding myelin basic protein in a randomized, placebo-controlled phase 1/2 trial
    Amit Bar-Or
    Montreal Neurological Institute, Montreal, Quebec, Canada
    Arch Neurol 64:1407-15. 2007
    ..To assess safety and immune modulation by BHT-3009, a tolerizing DNA vaccine encoding full-length human myelin basic protein, in patients with multiple sclerosis (MS)...
  89. ncbi request reprint Statins as potential therapeutic agents in neuroinflammatory disorders
    Olaf Stuve
    Department of Neurology, University of California, San Francisco, California 94143, USA
    Curr Opin Neurol 16:393-401. 2003
    ..In this article we will review those findings that indicate that statins may be beneficial in the treatment of multiple sclerosis, neurodegenerative disease, and ischemic stroke...
  90. ncbi request reprint Design of effective immunotherapy for human autoimmunity
    Marc Feldmann
    Kennedy Institute of Rheumatology, Faculty of Medicine, Imperial College School of Medicine, ARC Building, 1 Aspenlea Road, London W6 8LH, UK
    Nature 435:612-9. 2005
    ....
  91. ncbi request reprint Medicine: Collateral damage repaired
    Lawrence Steinman
    Nature 422:671-2. 2003
  92. pmc Heme oxygenase-1 and carbon monoxide suppress autoimmune neuroinflammation
    Angelo A Chora
    Instituto Gulbenkian de Ciencia, Oeiras, Portugal Departamento de Imunologia, Faculdade de Ciencias Medicas, Universidade Nova de Lisboa, Lisbon, Portugal
    J Clin Invest 117:438-47. 2007
    ..In conclusion, HO-1 or exposure to its end product CO counters autoimmune neuroinflammation and thus might be used therapeutically to treat MS...
  93. ncbi request reprint Drug Insight: using statins to treat neuroinflammatory disease
    Martin S Weber
    University of California San Francisco UCSF, CA 94143, USA
    Nat Clin Pract Neurol 1:106-12. 2005
    ....
  94. ncbi request reprint Involvement of both 'allergic' and 'autoimmune' mechanisms in EAE, MS and other autoimmune diseases
    Rosetta Pedotti
    Immunology and Muscular Pathology Unit, National Neurological Institute C Besta, Milan, 20133, Italy
    Trends Immunol 24:479-84. 2003
  95. ncbi request reprint Statins in the treatment of central nervous system autoimmune disease
    Martin S Weber
    Department of Neurology and Program in Immunology, University of California, San Francisco, USA
    J Neuroimmunol 178:140-8. 2006
    ..Based primarily upon the beneficial effects in EAE, statins are now being tested in patients in MS clinical trials...
  96. ncbi request reprint Antigen-specific therapies in multiple sclerosis: going beyond proteins and peptides
    Paulo Fontoura
    Department of Immunology, Faculty of Medical Sciences, New University of Lisbon, Portugal
    Int Rev Immunol 24:415-46. 2005
    ....
  97. ncbi request reprint Emerging therapeutic targets in multiple sclerosis
    Paulo Fontoura
    Department of Immunology, Faculty of Medical Sciences, New University of Lisbon, Lisbon, Portugal
    Curr Opin Neurol 19:260-6. 2006
    ..The aim of this review is to describe the recent findings regarding the pathogenesis of multiple sclerosis and their translation to new therapies...
  98. ncbi request reprint Type II monocytes modulate T cell-mediated central nervous system autoimmune disease
    Martin S Weber
    Department of Neurology and Program in Immunology, University of California, San Francisco, 513 Parnassus Avenue, S 268, San Francisco, California 94143 0435, USA
    Nat Med 13:935-43. 2007
    ..This demonstration of adoptive immunotherapy by type II monocytes identifies a central role for these cells in T cell immune modulation of autoimmunity...
  99. ncbi request reprint CD4+CD25+ regulatory T cells specific for a thymus-expressed antigen prevent the development of anaphylaxis to self
    Stefano Scabeni
    Immunology and Muscular Pathology Unit, Neurological Institute Foundation Carlo Besta, Milan, Italy
    J Immunol 180:4433-40. 2008
    ..These data indicate that naturally occurring CD4(+)CD25(+) Tregs specific for a peptide expressed under physiological conditions in the thymus are able to suppress the development of a systemic allergic reaction to self...
  100. ncbi request reprint Statins and their potential targets in multiple sclerosis therapy
    Olaf Stuve
    Department of Neurology, University of California, San Francisco, 521 Parnassus Avenue, C 440, San Francisco, CA 94143 0114, USA
    Expert Opin Ther Targets 7:613-22. 2003
    ..This article will outline experimental evidence that suggests potential clinical benefits of statins for MS patients...

Research Grants44

  1. IN VIVO TREATMENT OF EAE WITH ANTI I-A ANTIBODIES
    Lawrence Steinman; Fiscal Year: 1993
    ....
  2. Autoantibody Arrays Guide Tolergenic Therapy for Multiple Sclerosis
    Lawrence Steinman; Fiscal Year: 2010
    ..We shall develop strategies for tolerizing to proteins, lipids and carbohydrates of the myelin sheath. This approach may lead to better therapies to treat multiple sclerosis. ..
  3. IN VIVO TREATMENT OF EAE WITH ANTI I-A ANTIBODIES
    Lawrence Steinman; Fiscal Year: 2000
    ..Aim 5 is to assess the possibility of using DNA vaccination against TCR Vb for treatment of EAE. It is hoped that these studies will provide the basis for future clinical trials in MS patients. ..
  4. IN VIVO TREATMENT OF EAE WITH ANTI I-A ANTIBODIES
    Lawrence Steinman; Fiscal Year: 2000
    ..Aim 5 is to assess the possibility of using DNA vaccination against TCR Vb for treatment of EAE. It is hoped that these studies will provide the basis for future clinical trials in MS patients. ..
  5. IN VIVO TREATMENT OF EAE WITH ANTI I-A ANTIBODIES
    Lawrence Steinman; Fiscal Year: 1999
    ..Aim 5 is to assess the possibility of using DNA vaccination against TCR Vb for treatment of EAE. It is hoped that these studies will provide the basis for future clinical trials in MS patients. ..
  6. PEPTIDE MEDIATED IMMUNOTHERAPY FOR AUTOIMMUNE DISEASE
    Lawrence Steinman; Fiscal Year: 1993
    ..These approaches using therapeutic peptides could lead to the rational design of drugs for autoimmune disease...
  7. PEPTIDE MEDIATED IMMUNOTHERAPY FOR AUTOIMMUNE DISEASE
    Lawrence Steinman; Fiscal Year: 1992
    ..These approaches using therapeutic peptides could lead to the rational design of drugs for autoimmune disease...
  8. PEPTIDE MEDIATED IMMUNOTHERAPY FOR AUTOIMMUNE DISEASE
    Lawrence Steinman; Fiscal Year: 1991
    ..These approaches using therapeutic peptides could lead to the rational design of drugs for autoimmune disease...
  9. IN VIVO TREATMENT OF EAE WITH ANTI I-A ANTIBODIES
    Lawrence Steinman; Fiscal Year: 2001
    ..Aim 5 is to assess the possibility of using DNA vaccination against TCR Vb for treatment of EAE. It is hoped that these studies will provide the basis for future clinical trials in MS patients. ..
  10. PEPTIDE MEDIATED IMMUNOTHERAPY FOR AUTOIMMUNE DISEASE
    Lawrence Steinman; Fiscal Year: 2001
    ..This work with APL may be applicable not only to MS, but to other autoimmune diseases including juvenile diabetes, rheumatoid arthritis, and inflammatory bowel disease. ..
  11. Large Scale Images of Gene Transcription in MS and EAE
    Lawrence Steinman; Fiscal Year: 2002
    ..The discovery of the role of osteopontin, first identified in large scale profiles, exemplifies how this approach may help us to understand MS and to develop new therapies. ..
  12. Autoantibody Arrays Guide Tolergenic Therapy for Multiple Sclerosis
    Lawrence Steinman; Fiscal Year: 2009
    ..We shall develop strategies for tolerizing to proteins, lipids and carbohydrates of the myelin sheath. This approach may lead to better therapies to treat multiple sclerosis. ..
  13. MOLECULAR AND CELLULAR IMMUNOBIOLOGY
    Lawrence Steinman; Fiscal Year: 2007
    ..abstract_text> ..
  14. Large Scale Images of Gene Transcription in MS and EAE
    Lawrence Steinman; Fiscal Year: 2004
    ..The discovery of the role of osteopontin, first identified in large scale profiles, exemplifies how this approach may help us to understand MS and to develop new therapies. ..
  15. PEPTIDE MEDIATED IMMUNOTHERAPY FOR AUTOIMMUNE DISEASE
    Lawrence Steinman; Fiscal Year: 2003
    ..This work with APL may be applicable not only to MS, but to other autoimmune diseases including juvenile diabetes, rheumatoid arthritis, and inflammatory bowel disease. ..
  16. Large Scale Images of Gene Transcription in MS and EAE
    Lawrence Steinman; Fiscal Year: 2003
    ..The discovery of the role of osteopontin, first identified in large scale profiles, exemplifies how this approach may help us to understand MS and to develop new therapies. ..
  17. PEPTIDE MEDIATED IMMUNOTHERAPY FOR AUTOIMMUNE DISEASE
    Lawrence Steinman; Fiscal Year: 2002
    ..This work with APL may be applicable not only to MS, but to other autoimmune diseases including juvenile diabetes, rheumatoid arthritis, and inflammatory bowel disease. ..
  18. PEPTIDE MEDIATED IMMUNOTHERAPY FOR AUTOIMMUNE DISEASE
    Lawrence Steinman; Fiscal Year: 1990
    ..These approaches using therapeutic peptides could lead to the rational design of drugs for autoimmune disease...
  19. IN VIVO TREATMENT OF EAE WITH ANTI I-A ANTIBODIES
    Lawrence Steinman; Fiscal Year: 1999
    ..Aim 5 is to assess the possibility of using DNA vaccination against TCR Vb for treatment of EAE. It is hoped that these studies will provide the basis for future clinical trials in MS patients. ..
  20. PEPTIDE MEDIATED IMMUNOTHERAPY FOR AUTOIMMUNE DISEASE
    Lawrence Steinman; Fiscal Year: 1999
    ..This work with APL may be applicable not only to MS, but to other autoimmune diseases including juvenile diabetes, rheumatoid arthritis, and inflammatory bowel disease. ..
  21. IN VIVO TREATMENT OF EAE WITH ANTI I-A ANTIBODIES
    Lawrence Steinman; Fiscal Year: 1992
    ....
  22. IN VIVO TREATMENT OF EAE WITH ANTI I-A ANTIBODIES
    Lawrence Steinman; Fiscal Year: 1991
    ....
  23. IN VIVO TREATMENT OF EAE WITH ANTI I-A ANTIBODIES
    Lawrence Steinman; Fiscal Year: 1990
    ....
  24. PEPTIDE MEDIATED IMMUNOTHERAPY FOR AUTOIMMUNE DISEASE
    Lawrence Steinman; Fiscal Year: 2000
    ..This work with APL may be applicable not only to MS, but to other autoimmune diseases including juvenile diabetes, rheumatoid arthritis, and inflammatory bowel disease. ..