Howard Weiner

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. pmc Activated human CD4+CD45RO+ memory T-cells indirectly inhibit NLRP3 inflammasome activation through downregulation of P2X7R signalling
    Vanessa Beynon
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS ONE 7:e39576. 2012
  2. pmc Murine CD4 T cells produce a new form of TGF-β as measured by a newly developed TGF-β bioassay
    Takatoku Oida
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS ONE 6:e18365. 2011
  3. pmc In vivo induction of Tr1 cells via mucosal dendritic cells and AHR signaling
    Henry Yim Wu
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS ONE 6:e23618. 2011
  4. pmc IL-27 imparts immunoregulatory function to human NK cell subsets
    Alice Laroni
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS ONE 6:e26173. 2011
  5. pmc Induction of immunological tolerance by oral anti-CD3
    Andre Pires da Cunha
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Clin Dev Immunol 2012:425021. 2012
  6. pmc TGF-β induces surface LAP expression on murine CD4 T cells independent of Foxp3 induction
    Takatoku Oida
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, USA
    PLoS ONE 5:e15523. 2010
  7. ncbi request reprint Current issues in the treatment of human diseases by mucosal tolerance
    Howard L Weiner
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115 5817, USA
    Ann N Y Acad Sci 1029:211-24. 2004
  8. ncbi request reprint Immunology and immunotherapy of Alzheimer's disease
    Howard L Weiner
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nat Rev Immunol 6:404-16. 2006
  9. ncbi request reprint Multiple sclerosis is an inflammatory T-cell-mediated autoimmune disease
    Howard L Weiner
    Partners Multiple Sclerosis Center and Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Arch Neurol 61:1613-5. 2004
  10. ncbi request reprint Immunosuppressive treatment in multiple sclerosis
    Howard L Weiner
    Department of Neurology, Partners Multiple Sclerosis Center, Brigham and Women s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA
    J Neurol Sci 223:1-11. 2004

Research Grants

Detail Information

Publications95

  1. pmc Activated human CD4+CD45RO+ memory T-cells indirectly inhibit NLRP3 inflammasome activation through downregulation of P2X7R signalling
    Vanessa Beynon
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS ONE 7:e39576. 2012
    ..Thus, our data demonstrate that human P2X7R-mediated NLRP3 inflammasome activation is regulated by activated CD4+CD45RO+ memory T cells, and provide new information on the mechanisms mediating the therapeutic effects of IFNβ in MS...
  2. pmc Murine CD4 T cells produce a new form of TGF-β as measured by a newly developed TGF-β bioassay
    Takatoku Oida
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS ONE 6:e18365. 2011
    ..However, it is possible that active TGF-β from T cells may take a special form which is not detectable by ELISA...
  3. pmc In vivo induction of Tr1 cells via mucosal dendritic cells and AHR signaling
    Henry Yim Wu
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS ONE 6:e23618. 2011
    ..However, effective strategies that specifically induce Tr1 cells in vivo are limited. Furthermore, the pathways controlling the induction of these cells in vivo are not well understood...
  4. pmc IL-27 imparts immunoregulatory function to human NK cell subsets
    Alice Laroni
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS ONE 6:e26173. 2011
    ..Thus, understanding the role of IL-27 in NK cell function has important implications for treatment of autoimmune disorders...
  5. pmc Induction of immunological tolerance by oral anti-CD3
    Andre Pires da Cunha
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Clin Dev Immunol 2012:425021. 2012
    ..Here we review findings that identify a novel and powerful immunologic approach that is widely applicable for the treatment of human autoimmune conditions...
  6. pmc TGF-β induces surface LAP expression on murine CD4 T cells independent of Foxp3 induction
    Takatoku Oida
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, USA
    PLoS ONE 5:e15523. 2010
    ..Murine CD4 Foxp3(+) Tregs have also been reported to express surface LAP, but these studies have been hampered by the lack of suitable anti-mouse LAP mAbs...
  7. ncbi request reprint Current issues in the treatment of human diseases by mucosal tolerance
    Howard L Weiner
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115 5817, USA
    Ann N Y Acad Sci 1029:211-24. 2004
    ..The efficacy of mucosal tolerance has been clearly demonstrated in several animal models...
  8. ncbi request reprint Immunology and immunotherapy of Alzheimer's disease
    Howard L Weiner
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nat Rev Immunol 6:404-16. 2006
    ..New immunotherapies using humoral and cell-based approaches are currently being investigated for the treatment and prevention of Alzheimer's disease...
  9. ncbi request reprint Multiple sclerosis is an inflammatory T-cell-mediated autoimmune disease
    Howard L Weiner
    Partners Multiple Sclerosis Center and Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Arch Neurol 61:1613-5. 2004
  10. ncbi request reprint Immunosuppressive treatment in multiple sclerosis
    Howard L Weiner
    Department of Neurology, Partners Multiple Sclerosis Center, Brigham and Women s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA
    J Neurol Sci 223:1-11. 2004
    ..Cyclophosphamide and mitoxantrone are the most common immunosuppressive drugs used in patients with rapidly worsening MS whose disease is not controlled by beta-interferon or glatiramer acetate...
  11. ncbi request reprint A shift from adaptive to innate immunity: a potential mechanism of disease progression in multiple sclerosis
    Howard L Weiner
    Center for Neurologic Diseases, Dept of Neurology Brigham and Women s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Harvard Institute of Medicine 730, Boston, Massachusetts, 02115, USA
    J Neurol 255:3-11. 2008
    ....
  12. doi request reprint The challenge of multiple sclerosis: how do we cure a chronic heterogeneous disease?
    Howard L Weiner
    Partners Multiple Sclerosis Center, Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Ann Neurol 65:239-48. 2009
    ..There are three definitions of cure as it applies to MS: (1) halt progression of disease, (2) reverse neurological deficits, and (3) prevent MS. Although the pathways to each of these cures are linked, each requires a unique strategy...
  13. ncbi request reprint Oral administration of insulin to neonates suppresses spontaneous and cyclophosphamide induced diabetes in the NOD mouse
    R Maron
    Center for Neurologic Diseases, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115 5817, USA
    J Autoimmun 16:21-8. 2001
    ..Our findings that neonatal feeding of human insulin or insulin B-chain peptide is effective in inhibiting diabetes when given to the NOD mouse may have applications in preventing diabetes in high risk human populations...
  14. ncbi request reprint Treatment of multiple sclerosis with cyclophosphamide: critical review of clinical and immunologic effects
    H L Weiner
    Multiple Sclerosis Center, Brigham and Women s Hospital, Massachusetts General Hospital, Harvard Medical School, Boston 02115, USA
    Mult Scler 8:142-54. 2002
    ..Cyclophosphamide is currently used in patients whose disease is not controlled by beta-interferon or glatiramer acetate and those with rapidly worsening MS...
  15. pmc Oral tolerance
    Howard L Weiner
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    Immunol Rev 241:241-59. 2011
    ..A major avenue being investigated for the treatment of autoimmunity is the induction of Tregs and mucosal tolerance represents a non-toxic, physiologic approach to reach this goal...
  16. ncbi request reprint Neuroprotection by IL-10-producing MOG CD4+ T cells following ischemic stroke
    Dan Frenkel
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    J Neurol Sci 233:125-32. 2005
    ..Based on these results, modulation of cerebral inflammation by mucosal tolerance to myelin antigens may have applicability both as prophylactic therapy and treatment following ischemia attacks...
  17. ncbi request reprint Nasal vaccination with myelin oligodendrocyte glycoprotein reduces stroke size by inducing IL-10-producing CD4+ T cells
    Dan Frenkel
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    J Immunol 171:6549-55. 2003
    ..Modulation of cerebral inflammation by nasal vaccination with myelin Ags that increase IL-10 in the brain may improve outcome after stroke and enhance mechanisms of recovery...
  18. ncbi request reprint Cutting edge: oral type I IFN-tau promotes a Th2 bias and enhances suppression of autoimmune encephalomyelitis by oral glatiramer acetate
    Jeanne M Soos
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    J Immunol 169:2231-5. 2002
    ..This combination was associated with TGF-beta secretion and enhanced IL-10 production. Thus, IFN-tau is a potential candidate for use as a single agent or in combination therapy for multiple sclerosis...
  19. ncbi request reprint CD4+CD25- T cells that express latency-associated peptide on the surface suppress CD4+CD45RBhigh-induced colitis by a TGF-beta-dependent mechanism
    Takatoku Oida
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    J Immunol 170:2516-22. 2003
    ..The regulatory function of CD25(-)LAP(+) cells was abrogated in vivo by anti-TGF-beta mAb. These results identify a new TGF-beta-dependent regulatory CD4(+) T cell phenotype that is CD25(-) and LAP(+)...
  20. doi request reprint Accounting for disease modifying therapy in models of clinical progression in multiple sclerosis
    Brian C Healy
    Department of Neurology, Partners Multiple Sclerosis Center, Brigham and Women s Hospital, Harvard Medical School, Brookline, MA 02115, USA
    J Neurol Sci 303:109-13. 2011
    ..DMT modeling choice had a modest impact on the variables classified as predictors of EDSS score change. Importantly, however, interpretation of these predictors is dependent upon modeling choice...
  21. ncbi request reprint IFN-inducible protein 10/CXC chemokine ligand 10-independent induction of experimental autoimmune encephalomyelitis
    Robyn S Klein
    Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital East, Harvard Medical School, Building 149, 13th Street, Charlestown, MA 02129, USA
    J Immunol 172:550-9. 2004
    ..Our data demonstrated that IP-10 was not required for the trafficking of pathogenic T cells into the CNS in EAE but played an unexpected role in determining the threshold of disease susceptibility in the periphery...
  22. ncbi request reprint The ICOS molecule plays a crucial role in the development of mucosal tolerance
    Katsuichi Miyamoto
    Center for Neurologic Diseases, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    J Immunol 175:7341-7. 2005
    ..These results suggest that stimulating ICOS may provide an effective therapeutic approach for promoting mucosal tolerance...
  23. ncbi request reprint Mucosal administration of heat shock protein-65 decreases atherosclerosis and inflammation in aortic arch of low-density lipoprotein receptor-deficient mice
    Ruth Maron
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Mass, USA
    Circulation 106:1708-15. 2002
    ..Mucosal administration of autoantigens decreases organ-specific inflammation and disease in several models of autoimmunity (diabetes, arthritis, and encephalomyelitis) and is also being tested in human clinical trials...
  24. ncbi request reprint Inhibition of autoimmune diabetes by oral administration of anti-CD3 monoclonal antibody
    Hiroki Ishikawa
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Diabetes 56:2103-9. 2007
    ..Protection by oral anti-CD3 was transforming growth factor-beta dependent. Our results demonstrate that oral anti-CD3 is effective in the model of STZ-induced diabetes and may be a useful form of therapy for type 1 diabetes in humans...
  25. ncbi request reprint 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
    Ruth Maron
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA
    Int Immunol 14:131-8. 2002
    ....
  26. ncbi request reprint Oral CD3-specific antibody suppresses autoimmune encephalomyelitis by inducing CD4+ CD25- LAP+ T cells
    Hirofumi Ochi
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA
    Nat Med 12:627-35. 2006
    ..These findings identify a new immunologic approach that is widely applicable for the treatment of human autoimmune conditions...
  27. doi request reprint HLA-DR alleles in amyloid beta-peptide autoimmunity: a highly immunogenic role for the DRB1*1501 allele
    Victor Zota
    Center for Neurologic Diseases, Harvard Medical School and Brigham and Women s Hospital, Boston, MA, USA
    J Immunol 183:3522-30. 2009
    ..This new knowledge enables us to explore the basis for understanding the variations in naturally occurring Abeta-reactive T cells and Abeta immunogenicity among humans...
  28. ncbi request reprint Th3 cells in peripheral tolerance. I. Induction of Foxp3-positive regulatory T cells by Th3 cells derived from TGF-beta T cell-transgenic mice
    Yijun Carrier
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    J Immunol 178:179-85. 2007
    ..Thus, Ag-specific TGF-beta-producing Th3 cells play a crucial role in inducing and maintaining peripheral tolerance by driving the differentiation of Ag-specific Foxp3(+) regulatory cells in the periphery...
  29. ncbi request reprint Cyclophosphamide modulates CD4+ T cells into a T helper type 2 phenotype and reverses increased IFN-gamma production of CD8+ T cells in secondary progressive multiple sclerosis
    Arnon Karni
    Partners Multiple Sclerosis Center, Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA
    J Neuroimmunol 146:189-98. 2004
    ....
  30. ncbi request reprint Cutting Edge: Immature human dendritic cells express latency-associated peptide and inhibit T cell activation in a TGF-beta-dependent manner
    Roopali Gandhi
    Center for Neurologic Diseases, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    J Immunol 178:4017-21. 2007
    ..Taken together, our results indicate that surface expression of TGF-beta on DCs in association with LAP is one of the mechanisms by which immature DCs limit T cell activation and thus prevent autoimmune responses...
  31. doi request reprint A method for evaluating treatment switching criteria in multiple sclerosis
    Brian C Healy
    Partners Multiple Sclerosis Center, Department of Neurology, Brigham and Women s Hospital, Boston, MA, USA
    Mult Scler 16:1483-9. 2010
    ..We investigated a method to evaluate a treatment switching approach, namely treatment change after one multiple sclerosis (MS) relapse...
  32. pmc IL-27 is a key regulator of IL-10 and IL-17 production by human CD4+ T cells
    Gopal Murugaiyan
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    J Immunol 183:2435-43. 2009
    ..Our results demonstrate that IL-27 plays a key role in human T cells by promoting IL-10-secreting Tr1 cells and inhibiting Th17 cells and thus provides a dual regulatory mechanism to control autoimmunity and tissue inflammation...
  33. ncbi request reprint Inflammation and therapeutic vaccination in CNS diseases
    Howard L Weiner
    Center for Neurologic Diseases, Harvard Medical School and Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    Nature 420:879-84. 2002
    ..Such approaches, however, have the potential to induce unwanted inflammatory responses as well as to provide benefit...
  34. ncbi request reprint IL-23 is increased in dendritic cells in multiple sclerosis and down-regulation of IL-23 by antisense oligos increases dendritic cell IL-10 production
    Adi Vaknin-Dembinsky
    Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, MA 02115, USA
    J Immunol 176:7768-74. 2006
    ..Our results demonstrate that an abnormal Th1 bias in DCs from MS patients related to IL-23 exists, and that antisense oligonucleotides specific to IL-23 can be used for immune modulation by targeting DC gene expression...
  35. pmc Oral administration of OKT3 monoclonal antibody to human subjects induces a dose-dependent immunologic effect in T cells and dendritic cells
    Yaron Ilan
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    J Clin Immunol 30:167-77. 2010
    ..Oral administration of anti-CD3 has not been tested in humans, but suppresses autoimmunity in animal models. Beta-glucosylceramide enhances NKT cell and regulatory T cell activity and enhances the effects of oral anti-CD3 in animals...
  36. ncbi request reprint IL-10 is involved in the suppression of experimental autoimmune encephalomyelitis by CD25+CD4+ regulatory T cells
    Xingmin Zhang
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Int Immunol 16:249-56. 2004
    ....
  37. pmc Increased T cell reactivity to amyloid beta protein in older humans and patients with Alzheimer disease
    Alon Monsonego
    Center for Neurologic Diseases, Harvard Medical School and Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    J Clin Invest 112:415-22. 2003
    ....
  38. doi request reprint The impact of a recent relapse on patient-reported outcomes in subjects with multiple sclerosis
    Brian C Healy
    Partners Multiple Sclerosis Center, Brigham and Women s Hospital, 6th Floor, 1 Brookline Place, Brookline, MA 02445, USA
    Qual Life Res 21:1677-84. 2012
    ..In this study, we estimate the impact of a recent relapse on physical and mental health in subjects with relapsing-remitting multiple sclerosis (RRMS) using validated patient-reported outcome (PRO) measures...
  39. ncbi request reprint PD-1 ligands, negative regulators for activation of naive, memory, and recently activated human CD4+ T cells
    Guifang Cai
    Laboratory of Molecular Immunology, Department of Neurology, Brigham and Women s Hospital, Boston, MA 02115, USA
    Cell Immunol 230:89-98. 2004
    ..Together, our data demonstrated PD-1 functioned as a negative regulatory pathway on naive T cells during a primary response, and more potently, on memory or recently activated T cells during a secondary response...
  40. pmc In vitro induction of regulatory T cells by anti-CD3 antibody in humans
    Michal Abraham
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA
    J Autoimmun 30:21-8. 2008
    ..Thus, we have identified human T cells with strong in vitro regulatory properties induced in vitro by anti-CD3 which appear to act in a non-HLA restricted fashion by affecting antigen presenting cells...
  41. pmc Loss of functional suppression by CD4+CD25+ regulatory T cells in patients with multiple sclerosis
    Vissia Viglietta
    Laboratory of Molecular Immunology, Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    J Exp Med 199:971-9. 2004
    ..These data are the first to demonstrate alterations of CD4+CD25hi regulatory T cell function in patients with MS...
  42. ncbi request reprint Targeting monocyte recruitment in CNS autoimmune disease
    Leonid Izikson
    Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, Massachusetts, 02115, USA
    Clin Immunol 103:125-31. 2002
    ....
  43. pmc Reversal of axonal loss and disability in a mouse model of progressive multiple sclerosis
    Alexandre S Basso
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Clin Invest 118:1532-43. 2008
    ..Our data demonstrate the neuroprotective effect of treatment with a fullerene compound combined with a NMDA receptor antagonist, which may be useful in the treatment of progressive MS and other neurodegenerative diseases...
  44. ncbi request reprint Oral tolerance induced by continuous feeding: enhanced up-regulation of transforming growth factor-beta/interleukin-10 and suppression of experimental autoimmune encephalomyelitis
    Ana M C Faria
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    J Autoimmun 20:135-45. 2003
    ..Such feeding regimens may be advantageous in the application of oral tolerance for clinical purposes in the treatment of autoimmune and other inflammatory conditions...
  45. pmc Cutting edge: human latency-associated peptide+ T cells: a novel regulatory T cell subset
    Roopali Gandhi
    Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, MA 02115, USA
    J Immunol 184:4620-4. 2010
    ..In conclusion, we have characterized a novel population of human LAP(+) Tregs that is different from classic CD4(+)Foxp3(+)CD25(high) natural Tregs...
  46. pmc T and B cell hyperactivity and autoimmunity associated with niche-specific defects in apoptotic body clearance in TIM-4-deficient mice
    ROSELYNN RODRIGUEZ-MANZANET
    Department of Neurology, Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Harvard Institutes of Medicine, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 107:8706-11. 2010
    ....
  47. pmc Nasal vaccination with a proteosome-based adjuvant and glatiramer acetate clears beta-amyloid in a mouse model of Alzheimer disease
    Dan Frenkel
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Clin Invest 115:2423-33. 2005
    ..Our results identify a novel approach to immune therapy for AD that involves clearing of Abeta through the utilization of compounds that have been safely tested on or are currently in use in humans...
  48. pmc Nasal vaccination with troponin reduces troponin specific T-cell responses and improves heart function in myocardial ischemia-reperfusion injury
    Dan Frenkel
    Department of Neurology, Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    Int Immunol 21:817-29. 2009
    ..Modulation of cardiac inflammation by nasal troponin provides a novel treatment to decrease myocardial damage and enhance recovery after myocardial ischemia...
  49. pmc A randomized controlled double-masked trial of albuterol add-on therapy in patients with multiple sclerosis
    Samia J Khoury
    Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Arch Neurol 67:1055-61. 2010
    ..Albuterol sulfate, a β2-adrenergic agonist, reduces IL-12 expression, so we tested the effect of albuterol as an add-on treatment to glatiramer acetate therapy...
  50. ncbi request reprint Systems biology approaches for the study of multiple sclerosis
    Francisco J Quintana
    Center for Neurologic Diseases, Harvard Medical School, Boston, MA 02115, USA
    J Cell Mol Med 12:1087-93. 2008
    ....
  51. pmc Latency-associated peptide identifies a novel CD4+CD25+ regulatory T cell subset with TGFbeta-mediated function and enhanced suppression of experimental autoimmune encephalomyelitis
    Mei Ling Chen
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    J Immunol 180:7327-37. 2008
    ..Our work helps elucidate the ambiguity concerning the role of TGFbeta in CD4(+)CD25(+) Treg-mediated suppression and indicates that LAP is an authentic marker able to identify a TGFbeta-expressing CD4(+)CD25(+) Treg subset...
  52. pmc Predicting clinical progression in multiple sclerosis with the magnetic resonance disease severity scale
    Rohit Bakshi
    Department of Neurology, Brigham and Women s Hospital, Boston, MA 02115, USA
    Arch Neurol 65:1449-53. 2008
    ..Individual magnetic resonance imaging (MRI) disease severity measures, such as atrophy or lesions, show weak relationships to clinical status in patients with multiple sclerosis (MS)...
  53. doi request reprint Rate of brain atrophy in benign vs early multiple sclerosis
    Susan A Gauthier
    Department of Neurology, Partners Multiple Sclerosis Center, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, USA
    Arch Neurol 66:234-7. 2009
    ..Benign multiple sclerosis (MS) is defined by minimal or no disability after many years of observation, therefore a less degenerative disease process is suspected to be present in this subset of patients...
  54. ncbi request reprint Immunotherapeutic approaches to Alzheimer's disease
    Alon Monsonego
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Science 302:834-8. 2003
    ..We will also discuss how these approaches affect microglia activation, which plays a key role in therapy of such diseases...
  55. pmc Novel CD8+ Treg suppress EAE by TGF-beta- and IFN-gamma-dependent mechanisms
    Mei Ling Chen
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Eur J Immunol 39:3423-35. 2009
    ....
  56. pmc The role of the CD58 locus in multiple sclerosis
    Philip L De Jager
    Division of Molecular Immunology, Center for Neurologic Diseases, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 106:5264-9. 2009
    ....
  57. pmc 3 T MRI relaxometry detects T2 prolongation in the cerebral normal-appearing white matter in multiple sclerosis
    Mohit Neema
    Department of Neurology, Brigham and Women s Hospital, Laboratory for Neuroimaging Research, Partners MS Center, Harvard Medical School, Boston, MA 02445, USA
    Neuroimage 46:633-41. 2009
    ..Such findings may represent demyelination, inflammation, glial proliferation and axonal loss...
  58. pmc Adaptive autoimmunity and Foxp3-based immunoregulation in zebrafish
    Francisco J Quintana
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS ONE 5:e9478. 2010
    ..Recombinatorial mechanisms also operate in teleosts, but active immunoregulation is thought to be a late incorporation to the vertebrate lineage...
  59. pmc Meta-analysis of genome scans and replication identify CD6, IRF8 and TNFRSF1A as new multiple sclerosis susceptibility loci
    Philip L De Jager
    Division of Molecular Immunology, Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital and Harvard Medical School, Boston, MA, USA
    Nat Genet 41:776-82. 2009
    ....
  60. ncbi request reprint Microglia-mediated nitric oxide cytotoxicity of T cells following amyloid beta-peptide presentation to Th1 cells
    Alon Monsonego
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, HIM 730, Boston, MA 02115, USA
    J Immunol 171:2216-24. 2003
    ..Furthermore, Th2 type T cell responses may have a beneficial effect on this process by down-regulation of NO and the proinflammatory environment...
  61. ncbi request reprint Induction of oral tolerization in CD86 deficient mice: a role for CD86 and B cells in the up-regulation of TGF-beta
    Patricia A Gonnella
    Center for Neurologic Diseases, Brigham and Women s Hospital and Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA
    J Autoimmun 26:73-81. 2006
    ..These results demonstrate that CD86 is not required for oral tolerization and that both CD86 and B cells are important for the up-regulation of TGF-beta following oral antigen...
  62. pmc Mucosal anti-CD3 monoclonal antibody attenuates collagen-induced arthritis that is associated with induction of LAP+ regulatory T cells and is enhanced by administration of an emulsome-based Th2-skewing adjuvant
    Henry Yim Wu
    Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    J Immunol 185:3401-7. 2010
    ..These results demonstrate that mucosal anti-CD3 therapy may serve as a therapeutic approach in arthritis and that the biologic effect is enhanced by an emulsome-based adjuvant...
  63. ncbi request reprint Potential of beta2-adrenoceptor agonists as add-on therapy for multiple sclerosis: focus on salbutamol (albuterol)
    Karim Makhlouf
    Center for Neurologic Diseases, Brigham and Women s Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    CNS Drugs 16:1-8. 2002
    ..We conclude that salbutamol might be an interesting add-on therapy in patients with MS and that further research is warranted...
  64. ncbi request reprint Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells
    Estelle Bettelli
    Center for Neurologic Diseases, Beth Israel Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA
    Nature 441:235-8. 2006
    ..Our data demonstrate a dichotomy in the generation of pathogenic (T(H)17) T cells that induce autoimmunity and regulatory (Foxp3+) T cells that inhibit autoimmune tissue injury...
  65. ncbi request reprint Interferon-beta treatment alters peripheral blood monocytes chemokine production in MS patients
    Manuel Comabella
    Center for Neurologic Diseases, Brigham and Women s Hospital, 77 Avenue Louis Pasteur, HIM 714, Boston, MA 02115, USA
    J Neuroimmunol 126:205-12. 2002
    ..These findings suggest that IFN-beta treatment may have a differential affect on chemokine production by monocytes. Longitudinal studies must be done to confirm these observations...
  66. ncbi request reprint Feasibility and response to induction chemotherapy intensified with high-dose methotrexate for young children with newly diagnosed high-risk disseminated medulloblastoma
    Susan N Chi
    Division of Pediatric Oncology, New York University Medical Center, New York, NY, USA
    J Clin Oncol 22:4881-7. 2004
    ..To evaluate the feasibility of and response rate to an intensified induction chemotherapy regimen for young children with newly diagnosed high-risk or disseminated medulloblastomas...
  67. ncbi request reprint Magnetic resonance imaging surrogates of multiple sclerosis pathology and their relationship to central nervous system atrophy
    Dominik S Meier
    Center for Neurological Imaging, Partners Multiple Sclerosis Center, Brigham and Women s Hospital, Harvard Medical School, 221 Longwood Avenue, RFB 396, Boston, MA 02115, USA
    J Neuroimaging 14:46S-53S. 2004
    ..By exploiting the complementary nature and varying sensitivities of these magnetic resonance imaging surrogates, it is possible to create a more comprehensive picture of the degenerative process of multiple sclerosis...
  68. ncbi request reprint Time-series modeling of multiple sclerosis disease activity: a promising window on disease progression and repair potential?
    Dominik S Meier
    Center for Neurological Imaging, Department of Radiology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    Neurotherapeutics 4:485-98. 2007
    ....
  69. ncbi request reprint A dominant function for interleukin 27 in generating interleukin 10-producing anti-inflammatory T cells
    Amit Awasthi
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Cambridge, Massachusetts 02139, USA
    Nat Immunol 8:1380-9. 2007
    ..Thus, IL-27 and transforming growth factor-beta promote the generation of IL-10-producing Tr1 cells...
  70. ncbi request reprint Recovery from experimental allergic encephalomyelitis is TGF-beta dependent and associated with increases in CD4+LAP+ and CD4+CD25+ T cells
    Xingmin Zhang
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    Int Immunol 18:495-503. 2006
    ..Taken together, our results demonstrate that both CD4+CD25+ and CD4+LAP+ regulatory T cells mediate recovery from PLP 139-151-induced EAE in SJL mice in which TGF-beta plays an important role...
  71. pmc Cytometric profiling in multiple sclerosis uncovers patient population structure and a reduction of CD8low cells
    Philip L De Jager
    Harvard Medical School Partners Center for Genomics and Genetics, Brigham and Women s Hospital, 77 Avenue Louis Pasteur, NRB 168C, Boston, MA 02115, USA
    Brain 131:1701-11. 2008
    ....
  72. ncbi request reprint The mechanism of nasal tolerance in lupus prone mice is T-cell anergy induced by immature B cells that lack B7 expression
    Henry Yim Wu
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA
    J Autoimmun 26:116-26. 2006
    ..The anergic T cells do not possess suppressive function in coculture with naïve responder T cells nor produce suppressive cytokines interleukin 10 and transforming growth factor-beta in vitro...
  73. ncbi request reprint Oral tolerance
    Henry Yim Wu
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Immunol Res 28:265-84. 2003
    ..This type of immunological event is termed oral tolerance. In this review, we examine the mechanisms behind the induction of oral tolerance and provide findings from its use as a form of treatment for autoimmune diseases...
  74. ncbi request reprint Induction of low dose oral tolerance in IL-10 deficient mice with experimental autoimmune encephalomyelitis
    Patricia A Gonnella
    Center for Neurologic Diseases, Brigham and Women s Hospital and Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA
    J Autoimmun 23:193-200. 2004
    ..These results demonstrate that IL-10 is not required for the induction of low dose oral tolerance but is required for the regulation of INF-gamma which affects severity of disease in tolerized mice...
  75. pmc An endogenous aryl hydrocarbon receptor ligand acts on dendritic cells and T cells to suppress experimental autoimmune encephalomyelitis
    Francisco J Quintana
    Center for Neurologic Diseases, The Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 107:20768-73. 2010
    ....
  76. ncbi request reprint Intense immunosuppression in patients with rapidly worsening multiple sclerosis: treatment guidelines for the clinician
    Aaron Boster
    The Multiple Sclerosis Clinical Research Center, Department of Neurology, Wayne State University School of Medicine, and The Detroit Medical Center, Detroit, MI 48201, USA
    Lancet Neurol 7:173-83. 2008
    ..This Review describes the use of intense immunosuppressant drugs and natalizumab in patients with rapidly worsening MS and provides clinicians with guidelines for the use of these drugs in this patient group...
  77. pmc Smoking and disease progression in multiple sclerosis
    Brian C Healy
    Department of Neurology, Partners MS Center, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, USA
    Arch Neurol 66:858-64. 2009
    ..Although cigarette smokers are at increased risk of developing multiple sclerosis (MS), the effect of smoking on the progression of MS remains uncertain...
  78. ncbi request reprint Mesenteric lymph nodes are critical for the induction of high-dose oral tolerance in the absence of Peyer's patches
    Thomas W Spahn
    Department of Medicine B, Westfalische Wilhelms Universitat, Munster, Germany
    Eur J Immunol 32:1109-13. 2002
    ..Taken collectively, the data show that in the presence of MLN PP are not required for OT induction and that the presence of MLN is sufficient for OT induction in the LTalpha-/- model...
  79. ncbi request reprint Induction of medulloblastomas in mice by sonic hedgehog, independent of Gli1
    Howard L Weiner
    Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, New York 10016, USA
    Cancer Res 62:6385-9. 2002
    ..We have developed an efficient mouse model of medulloblastoma and shown that Gli1 is not required for tumorigenesis when Shh signaling is activated upstream in the pathway...
  80. pmc Abeta-induced meningoencephalitis is IFN-gamma-dependent and is associated with T cell-dependent clearance of Abeta in a mouse model of Alzheimer's disease
    Alon Monsonego
    National Institute of Biotechnology and Department of Microbiology and Immunology, Faculty of Health Sciences, Ben Gurion University, Beer Sheva 84105, Israel
    Proc Natl Acad Sci U S A 103:5048-53. 2006
    ....
  81. ncbi request reprint Induction of low dose oral tolerance in monocyte chemoattractant protein-1- and CCR2-deficient mice
    Patricia A Gonnella
    Center for Neurologic Diseases, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    J Immunol 170:2316-22. 2003
    ..These results demonstrate that MCP-1 is not required for induction of oral tolerance and that MCP-1 and CCR2 are essential for up-regulation of IL-4 in tolerized mice...
  82. ncbi request reprint IL-18 is linked to raised IFN-gamma in multiple sclerosis and is induced by activated CD4(+) T cells via CD40-CD40 ligand interactions
    Arnon Karni
    Center for Neurologic Diseases, Brigham and Women s and Massachusetts General Hospitals, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA
    J Neuroimmunol 125:134-40. 2002
    ..These results demonstrated that IL-18 has an important role in augmenting Th-1 type immune responses in MS and may be involved in immune changes that occur when patients enter the progressive stage...
  83. ncbi request reprint Beneficial effect of orally administered myelin basic protein in EAE-susceptible Lewis rats in a model of acute CNS degeneration
    Alon Monsonego
    Department of Neurobiology, The Weizmann Institute of Science, 76100 Rehovot, Israel
    J Autoimmun 21:131-8. 2003
    ..Oral immunization with MBP can be viewed as a way to control the autoimmunity capable of fighting off the consequences of CNS injury in EAE-susceptible strains...
  84. ncbi request reprint Gelatinases (MMP-2 and MMP-9) are preferentially expressed by Th1 vs. Th2 cells
    Michal Abraham
    Neuroimmunology Research Unit, Carmel Medical Center, Haifa, Israel
    J Neuroimmunol 163:157-64. 2005
    ....
  85. ncbi request reprint Medulloblastoma: mouse models and novel targeted therapies based on the Sonic hedgehog pathway
    Leandro R Piedimonte
    Division of Pediatric Neurosurgery, Department of Neurosurgery, New York University School of Medicine, New York, New York 10016, USA
    Neurosurg Focus 19:E8. 2005
    ..In this review the authors discuss the mouse models based on the Sonic hedgehog pathway, which have provided a better knowledge of the genetic and molecular alterations of medulloblastoma...
  86. ncbi request reprint Development of a safe oral Abeta vaccine using recombinant adeno-associated virus vector for Alzheimer's disease
    Hideo Hara
    National Institute for Longevity Sciences, NCGG, 36 3 Gengo, Morioka, Obu City, Aichi 474 8522, Japan
    J Alzheimers Dis 6:483-8. 2004
    ..Brain Abeta burden was significantly decreased compared to the control without inflammatory changes. This oral AAV/Abeta vaccine seems to be promising for prevention and treatment of Alzheimer's disease...
  87. ncbi request reprint TGF-beta-mediated suppression by CD4+CD25+ T cells is facilitated by CTLA-4 signaling
    Takatoku Oida
    Mucosal Immunity Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, USA
    J Immunol 177:2331-9. 2006
    ..This suggests that CTLA-4 signaling facilitates TGF-beta-mediated suppression by intensifying the TGF-beta signal at the point of suppressor cell-target cell interaction...
  88. ncbi request reprint Oral tolerance and TGF-beta-producing cells
    Ana M C Faria
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur Him 730, Boston, MA 02115, USA
    Inflamm Allergy Drug Targets 5:179-90. 2006
    ..Thus, it appears that TGF-beta-producing cells are not only crucial for oral tolerance, but they may be master regulators of most of the mechanisms triggered by antigen feeding...
  89. pmc Oral tolerance: therapeutic implications for autoimmune diseases
    Ana M C Faria
    Departamento de Bioquimica e Imunologia, Instituto de Ciencias Biologicas, Universidade Federal de Minas Gerais, Av Antonio Carlos, 6627, Belo Horizonte, MG 31270 901, Brazil
    Clin Dev Immunol 13:143-57. 2006
    ....
  90. ncbi request reprint Th3 cells in peripheral tolerance. II. TGF-beta-transgenic Th3 cells rescue IL-2-deficient mice from autoimmunity
    Yijun Carrier
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    J Immunol 178:172-8. 2007
    ....
  91. doi request reprint Regulating rejection with cell therapy
    Mohamed H Sayegh
    Nat Biotechnol 26:191-2. 2008
  92. pmc Membrane bound IL-15 is increased on CD14 monocytes in early stages of MS
    Adi Vaknin-Dembinsky
    Center for Neurological Diseases, Brigham and Women s Hospital, Harvard Medical, School, Boston Massachusetts 02115, United States
    J Neuroimmunol 195:135-9. 2008
    ..Thus, IL-15 may be an important cytokine that drives Th1 responses early in the course of the disease and could serve as a target for immunotherapy and as an early marker in the immunologic staging of MS...
  93. ncbi request reprint Serial blood T cell repertoire alterations in multiple sclerosis patients; correlation with clinical and MRI parameters
    David Axel Laplaud
    Institut National de la Santé Et de la Recherche Médicale Unité 643 Immunointervention dans les allo et Xénotransplantations, Institut de Transplantation et de Recherche en Transplantation CHU Hôtel Dieu, 30 Bd Jean Monnet, 44093 Nantes Cedex, France
    J Neuroimmunol 177:151-60. 2006
    ..36, p=0.05). These findings which need confirmation on larger serial cohorts, suggest an association between the magnitude of TCRBV CDR3 length distribution alterations in the peripheral blood of MS patients and the disease process...
  94. doi request reprint Novel therapeutic strategies for multiple sclerosis--a multifaceted adversary
    Rocio S Lopez-Diego
    Department of Neurology, Harvard Medical School, Brigham and Women s Hospital, Harvard Institute of Medicine Room 730, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA
    Nat Rev Drug Discov 7:909-25. 2008
    ....
  95. pmc Oral tolerance
    Ana M C Faria
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Immunol Rev 206:232-59. 2005
    ....

Research Grants33

  1. Mucosal Immunotherapy in a mouse model of Alzheimer's Disease
    Howard L Weiner; Fiscal Year: 2010
    ..In this aim, we will investigate long term mucosal strategy to prevent and treat APP Tg mice using unique mucosal adjuvant combination given nasally and their ability to enhance amyloid clearance. ..
  2. IMMUNOREGULATORY T CELLS IN MULTIPLE SCLEROSIS
    Howard Weiner; Fiscal Year: 2004
    ..Our investigations will be greatly facilitated by our new Multiple Sclerosis Center with a large patient base and a dedicated MS MRI magnet and image analysis laboratory. ..
  3. MECHANISMS OF THE INDUCTION OF ORAL TOLERANCE
    Howard Weiner; Fiscal Year: 2000
    ....
  4. IMMUNOREGULATORY T-CELLS IN MULTIPLE SCLEROSIS
    Howard Weiner; Fiscal Year: 1993
    ....
  5. IMMUNOREGULATORY T-CELLS IN MULTIPLE SCLEROSIS
    Howard Weiner; Fiscal Year: 1992
    ....
  6. IMMUNOREGULATORY T-CELLS IN MULTIPLE SCLEROSIS
    Howard Weiner; Fiscal Year: 1990
    ....
  7. MECHANISMS OF THE INDUCTION OF ORAL TOLERANCE
    Howard Weiner; Fiscal Year: 2005
    ..Th2/3 responses and their effect on the EAE model. The application has been re-revised in accordance with the reviewer's critiques with special attention to specific aim 1. ..
  8. MECHANISMS OF THE INDUCTION OF ORAL TOLERANCE
    Howard Weiner; Fiscal Year: 1999
    ....
  9. MECHANISMS OF THE INDUCTION OF ORAL TOLERANCE
    Howard Weiner; Fiscal Year: 2009
    ..We will investigate basic mechanisms of two unique adjuvants that we have found to be orally active and that polarize towards Thl vs. Th2/3 responses and their effect on the EAE model. ..
  10. Mucosal Immunotherapy in a mouse model of Alzheimer's Disease
    Howard Weiner; Fiscal Year: 2007
    ..In this aim, we will investigate long term mucosal strategy to prevent and treat APP Tg mice using unique mucosal adjuvant combination given nasally and their ability to enhance amyloid clearance. ..
  11. MECHANISMS OF THE INDUCTION OF ORAL TOLERANCE
    Howard Weiner; Fiscal Year: 2007
    ..Th2/3 responses and their effect on the EAE model. The application has been re-revised in accordance with the reviewer's critiques with special attention to specific aim 1. ..
  12. Mucosal Immunotherapy in a mouse model of Alzheimer's Disease
    Howard Weiner; Fiscal Year: 2006
    ..In this aim, we will investigate long term mucosal strategy to prevent and treat APP Tg mice using unique mucosal adjuvant combination given nasally and their ability to enhance amyloid clearance. ..
  13. MECHANISMS OF THE INDUCTION OF ORAL TOLERANCE
    Howard Weiner; Fiscal Year: 2006
    ..Th2/3 responses and their effect on the EAE model. The application has been re-revised in accordance with the reviewer's critiques with special attention to specific aim 1. ..
  14. Mucosal Immunotherapy in a mouse model of Alzheimer's Disease
    Howard Weiner; Fiscal Year: 2009
    ..In this aim, we will investigate long term mucosal strategy to prevent and treat APP Tg mice using unique mucosal adjuvant combination given nasally and their ability to enhance amyloid clearance. ..
  15. IMMUNOREGULATORY T CELLS IN MULTIPLE SCLEROSIS
    Howard Weiner; Fiscal Year: 2005
    ..Our investigations will be greatly facilitated by our new Multiple Sclerosis Center with a large patient base and a dedicated MS MRI magnet and image analysis laboratory. ..
  16. IMMUNOREGULATORY T CELLS IN MULTIPLE SCLEROSIS
    Howard Weiner; Fiscal Year: 2003
    ..Our investigations will be greatly facilitated by our new Multiple Sclerosis Center with a large patient base and a dedicated MS MRI magnet and image analysis laboratory. ..
  17. IMMUNOREGULATORY T CELLS IN MULTIPLE SCLEROSIS
    Howard Weiner; Fiscal Year: 1999
    ..cells? 6) is there a genetic linkage of increased anti-CD3 induced IL-12/IFN-g in first degree relatives? 7) is there any link between these findings and disease type and stage in patients followed serially and in response to therapy? ..
  18. IMMUNOREGULATORY T-CELLS IN MULTIPLE SCLEROSIS
    Howard Weiner; Fiscal Year: 1991
    ....
  19. IMMUNOREGULATORY T CELLS IN MULTIPLE SCLEROSIS
    Howard Weiner; Fiscal Year: 2000
    ..cells? 6) is there a genetic linkage of increased anti-CD3 induced IL-12/IFN-g in first degree relatives? 7) is there any link between these findings and disease type and stage in patients followed serially and in response to therapy? ..
  20. MECHANISMS OF THE INDUCTION OF ORAL TOLERANCE
    Howard Weiner; Fiscal Year: 2001
    ....
  21. MECHANISMS OF THE INDUCTION OF ORAL TOLERANCE
    Howard Weiner; Fiscal Year: 2002
    ....
  22. IMMUNOREGULATORY T CELLS IN MULTIPLE SCLEROSIS
    Howard Weiner; Fiscal Year: 2002
    ..Our investigations will be greatly facilitated by our new Multiple Sclerosis Center with a large patient base and a dedicated MS MRI magnet and image analysis laboratory. ..