Suhayl Dhib-Jalbut

Summary

Affiliation: New Jersey
Country: USA

Publications

  1. ncbi request reprint Neurodegeneration and neuroprotection in multiple sclerosis and other neurodegenerative diseases
    Suhayl Dhib-Jalbut
    UMDNJ Robert Wood Johnson Medical School, New Brunswick, NJ 08901, and The Cleveland Clinic, OH, USA
    J Neuroimmunol 176:198-215. 2006
  2. doi request reprint HLA DR and DQ alleles and haplotypes associated with clinical response to glatiramer acetate in multiple sclerosis
    Suhayl Dhib-Jalbut
    Department of Neurology, UMDNJ Robert Wood Johnson Medical School, 683 Hoes Lane, Piscataway, NJ 08554, USA Electronic address
    Mult Scler Relat Disord 2:340-8. 2013
  3. doi request reprint Immune response during interferon beta-1b treatment in patients with multiple sclerosis who experienced relapses and those who were relapse-free in the START study
    Suhayl Dhib-Jalbut
    UMDNJ Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA
    J Neuroimmunol 254:131-40. 2013
  4. doi request reprint Interferon-beta mechanisms of action in multiple sclerosis
    Suhayl Dhib-Jalbut
    University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick, NJ 08901 2160, USA
    Neurology 74:S17-24. 2010
  5. ncbi request reprint Delivery of transgenically modified adult bone marrow cells to the rodent central nervous system
    Suhayl Dhib-Jalbut
    Department of Neurology, University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA
    Expert Opin Biol Ther 4:669-75. 2004
  6. ncbi request reprint Pathogenesis of myelin/oligodendrocyte damage in multiple sclerosis
    Suhayl Dhib-Jalbut
    Department of Neurology, University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, New Brunswick, NJ 08901 2160, USA
    Neurology 68:S13-21; discussion S43-54. 2007
  7. doi request reprint Hematopoietic progenitors express myelin basic protein and ensheath axons in Shiverer brain
    James Goolsby
    Department of Neurology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    J Neuroimmunol 257:13-20. 2013
  8. pmc Multiple sclerosis-linked and interferon-beta-regulated gene expression in plasmacytoid dendritic cells
    Latt Latt Aung
    Department of Neurology, Robert Wood Johnson Medical School, New Brunswick, NJ 08901, United States
    J Neuroimmunol 250:99-105. 2012
  9. doi request reprint IL-27: a potential biomarker for responders to glatiramer acetate therapy
    John E Mindur
    Department of Neurology, Rutgers Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA
    J Neuroimmunol . 2016
  10. doi request reprint Immunologic aspects of multiple sclerosis
    Sridhar Boppana
    Department of Neurology, University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, Piscataway, NJ, USA
    Mt Sinai J Med 78:207-20. 2011

Research Grants

  1. INTERFERON-B AND COPOLYMER-I IN MULTIPLE SCLEROSIS.
    Suhayl Dhib Jalbut; Fiscal Year: 2003

Collaborators

Detail Information

Publications26

  1. ncbi request reprint Neurodegeneration and neuroprotection in multiple sclerosis and other neurodegenerative diseases
    Suhayl Dhib-Jalbut
    UMDNJ Robert Wood Johnson Medical School, New Brunswick, NJ 08901, and The Cleveland Clinic, OH, USA
    J Neuroimmunol 176:198-215. 2006
    ..Elucidating the mechanisms that orchestrate neuronal diseases should facilitate development of neuroprotective and neurorestorative strategies...
  2. doi request reprint HLA DR and DQ alleles and haplotypes associated with clinical response to glatiramer acetate in multiple sclerosis
    Suhayl Dhib-Jalbut
    Department of Neurology, UMDNJ Robert Wood Johnson Medical School, 683 Hoes Lane, Piscataway, NJ 08554, USA Electronic address
    Mult Scler Relat Disord 2:340-8. 2013
    ..Currently, there are no validated biomarkers of clinical response to any of the approved treatments for MS. The objective of this study was to determine if HLA-class II alleles predict the clinical response to glatiramer acetate (GA)...
  3. doi request reprint Immune response during interferon beta-1b treatment in patients with multiple sclerosis who experienced relapses and those who were relapse-free in the START study
    Suhayl Dhib-Jalbut
    UMDNJ Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA
    J Neuroimmunol 254:131-40. 2013
    ..CXCR3+CD8+ T-cells tended to be higher but declined with treatment in relapse-free compared with relapsing subjects. Findings show the potential of cytokine and neurotrophic factors as biomarkers of clinical response to IFNβ-1b...
  4. doi request reprint Interferon-beta mechanisms of action in multiple sclerosis
    Suhayl Dhib-Jalbut
    University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick, NJ 08901 2160, USA
    Neurology 74:S17-24. 2010
    ..All these mechanisms are believed to underlie the therapeutic effect of IFNbeta in the treatment of RRMS...
  5. ncbi request reprint Delivery of transgenically modified adult bone marrow cells to the rodent central nervous system
    Suhayl Dhib-Jalbut
    Department of Neurology, University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA
    Expert Opin Biol Ther 4:669-75. 2004
    ..This article, which is focused on work from the authors' research, reviews the opportunities and difficulties presented by this approach...
  6. ncbi request reprint Pathogenesis of myelin/oligodendrocyte damage in multiple sclerosis
    Suhayl Dhib-Jalbut
    Department of Neurology, University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, New Brunswick, NJ 08901 2160, USA
    Neurology 68:S13-21; discussion S43-54. 2007
    ....
  7. doi request reprint Hematopoietic progenitors express myelin basic protein and ensheath axons in Shiverer brain
    James Goolsby
    Department of Neurology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    J Neuroimmunol 257:13-20. 2013
    ..We demonstrate that adult wild-type mouse bone marrow stem cells can express MBP and ensheath axons when transplanted into Shiverer brain...
  8. pmc Multiple sclerosis-linked and interferon-beta-regulated gene expression in plasmacytoid dendritic cells
    Latt Latt Aung
    Department of Neurology, Robert Wood Johnson Medical School, New Brunswick, NJ 08901, United States
    J Neuroimmunol 250:99-105. 2012
    ..We have identified 60 genes which were abnormally expressed in MS patients and were corrected after treatment. These genes could be studied as potential MS biomarkers and possible therapeutic targets in MS...
  9. doi request reprint IL-27: a potential biomarker for responders to glatiramer acetate therapy
    John E Mindur
    Department of Neurology, Rutgers Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA
    J Neuroimmunol . 2016
    ....
  10. doi request reprint Immunologic aspects of multiple sclerosis
    Sridhar Boppana
    Department of Neurology, University of Medicine and Dentistry of New Jersey Robert Wood Johnson Medical School, Piscataway, NJ, USA
    Mt Sinai J Med 78:207-20. 2011
    ..The mechanism of action of approved and experimental therapies, and how these mechanisms support the immunopathogenesis paradigm, is also reviewed...
  11. pmc Interferon-β inhibits toll-like receptor 9 processing in multiple sclerosis
    KONSTANTIN E BALASHOV
    Department of Neurology, University of Medicine and Dentistry, New Jersey Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA
    Ann Neurol 68:899-906. 2010
    ..In the animal model of MS, TLR9 agonists can induce disease. We hypothesized that pDCs are inhibited by disease-modifying therapy such as interferon (IFN)-β, consequently decreasing the frequency of MS attacks...
  12. pmc Cytokine changes during interferon-beta therapy in multiple sclerosis: correlations with interferon dose and MRI response
    Jerome J Graber
    University of Maryland School of Medicine, Department of Neurology, MD, USA
    J Neuroimmunol 185:168-74. 2007
    ..013). This is the first study that compares cytokine changes between the two IFN-beta regimes and demonstrates that serum IL-10 levels decrease in those patients who continue to have active MRI lesions while on interferon-beta therapy...
  13. doi request reprint Biomarkers of disease activity in multiple sclerosis
    Jerome J Graber
    Department of Neurology, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    J Neurol Sci 305:1-10. 2011
    ..The heterogeneity of multiple sclerosis may necessitate individualized biomarkers and therapeutic decisions within distinct subsets of patients...
  14. ncbi request reprint IFN-beta gene transfer into the central nervous system using bone marrow cells as a delivery system
    Tapas Kumar Makar
    Department of Neurology, University of Maryland, and Department of Veterans Affairs, Baltimore, MD 21201, USA
    J Interferon Cytokine Res 22:783-91. 2002
    ....
  15. pmc Plasmacytoid dendritic cells in multiple sclerosis: chemokine and chemokine receptor modulation by interferon-beta
    Latt Latt Aung
    Department of Neurology, UMDNJ RWJMS, New Brunswick, NJ 08901, USA
    J Neuroimmunol 226:158-64. 2010
    ..This finding represents a new immunomodulatory effect of IFN-beta in patients with multiple sclerosis...
  16. pmc MMP-9 expression is increased in B lymphocytes during multiple sclerosis exacerbation and is regulated by microRNA-320a
    Latt Latt Aung
    Department of Neurology, Rutgers Robert Wood Johnson Medical School, 125 Paterson Street, New Brunswick, NJ 08901, United States
    J Neuroimmunol 278:185-9. 2015
    ..In summary, expression of miR-320a is decreased in B cells of MS patients and may contribute to increased blood-brain barrier permeability and neurological disability. ..
  17. doi request reprint Comparison of IFN-β inducible gene expression in primary-progressive and relapsing-remitting multiple sclerosis
    Sridhar Boppana
    Department of Neurology, Rutgers Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA
    J Neuroimmunol 265:68-74. 2013
    ..This data suggests HLA-G to be a possible candidate gene found impaired in IFN-β-mediated immune regulation in PPMS patients. ..
  18. pmc Acute multiple sclerosis lesion: conversion of restricted diffusion due to vasogenic edema
    KONSTANTIN E BALASHOV
    Department of Neurology, UMDNJ Robert Wood Johnson Medical School, New Brunswick, New Jersey 08901, USA
    J Neuroimaging 21:202-4. 2011
    ..The implications of decreased diffusion in the acute phase of MS lesions for the disease pathogenesis are discussed...
  19. doi request reprint Advances in the immunopathogenesis of multiple sclerosis
    Sudhir K Yadav
    Department of Neurology, Rutgers Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA
    Curr Opin Neurol 28:206-19. 2015
    ..This review addresses the current mechanisms of immune dysregulation in the development of multiple sclerosis, including the impact of environmental risk factors on immunity in both multiple sclerosis and its animal models...
  20. pmc Early treatment with anti-VLA-4 mAb can prevent the infiltration and/or development of pathogenic CD11b+CD4+ T cells in the CNS during progressive EAE
    John E Mindur
    Department of Neurology, Rutgers Robert Wood Johnson Medical School, Piscataway, New Jersey, United States of America
    PLoS ONE 9:e99068. 2014
    ..Collectively, our data suggest that early treatment with anti-VLA-4 mAb can provide neuroprotection against progressive CNS autoimmune disease by preventing the accumulation of pathogenic GM-CSF-producing CD11b+CD4+ T cells in the CNS. ..
  21. doi request reprint Effect of interferon beta-1a on B7.1 and B7.2 B-cell expression and its impact on T-cell proliferation
    Hui Huang
    Department of Neurology, UMDNJ Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA
    J Neuroimmunol 258:27-31. 2013
    ..These data suggest that IFN β-1a and B cells can interact to play a beneficial role in the treatment of multiple sclerosis...
  22. ncbi request reprint Mechanisms of action of interferons and glatiramer acetate in multiple sclerosis
    Suhayl Dhib-Jalbut
    Department of Neurology, University of Maryland School of Medicine, Baltimore VA Medical Center, Baltimore, MD, USA
    Neurology 58:S3-9. 2002
    ..IFN beta has no direct effects in the CNS, but glatiramer acetate-specific T cells are believed to have access to the CNS, where they can exert anti-inflammatory and possibly neuroprotective effects...
  23. pmc Hematopoietic progenitors express neural genes
    James Goolsby
    Department of Neurology, University of Maryland School of Medicine, and Multiple Sclerosis Center of Excellence, Veterans Affairs Medical Center, Baltimore, MD 21201, USA
    Proc Natl Acad Sci U S A 100:14926-31. 2003
    ..The fact that these CD34+ cells also express transcription factors (Rex-1 and Oct-4) that are found in early development elicits the hypothesis that they may be pluripotent embryonic-like stem cells...
  24. ncbi request reprint Bystander modulation of chemokine receptor expression on peripheral blood T lymphocytes mediated by glatiramer therapy
    Rameeza Allie
    Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Arch Neurol 62:889-94. 2005
    ..Determining the site of action and effect of glatiramer on cell trafficking is of major importance in designing rational combination therapy clinical trials...
  25. doi request reprint Protective autoimmunity in the nervous system
    Jerome J Graber
    New York University School of Medicine, Department of Neurology, New York, NY, USA
    Pharmacol Ther 121:147-59. 2009
    ..The beneficent aspects of the immune response in the nervous system are beginning to be appreciated and their potential as pharmacologic targets in neurologic disease is being explored...
  26. ncbi request reprint Defective NF-kappaB activation in virus-infected neuronal cells is restored by genetic complementation
    Yu Yan Fang
    Department of Neurology, University of Maryland at Baltimore, and Department of Veterans Affairs, Baltimore, Maryland, USA
    J Neurovirol 8:459-63. 2002
    ..These results indicate that failure of MV to activate neuronal NF-kappaB is due to a signaling defect and that MV utilizes an NF-kappaB signaling pathway distinct from that of TNFalpha, but may overlap with that for IL-1 and LPS...

Research Grants1

  1. INTERFERON-B AND COPOLYMER-I IN MULTIPLE SCLEROSIS.
    Suhayl Dhib Jalbut; Fiscal Year: 2003
    ..The proposed research could help identify components of the immunologic network in MS that are associated with response to treatment, and therefore help in the design of more effective future therapies. ..