Bio

Bio


Jeffrey Dunn, MD, FAAN serves as Professor of Clinical Neurology and Division Chief of Clinical Neuroimmunology in the Department of Neurology and Neurosciences at Stanford University. His clinical focus is conditions in which the immune system interacts with the central nervous system to cause disease. His research employs a collaborative interdisciplinary approach to identify biomarkers of disease status, and to identify potential therapeutic targets for novel drug development. Dr. Dunn has served as Principal Investigator in more than 20 clinical trials of new and emerging treatments for MS, many of which have since been FDA approved for use. Dr. Dunn is an elected Fellow and Vice Chair of the Executive Committee of the MS Section of the American Academy of Neurology. He has been awarded the prestigious Henry J. Kaiser Family Foundation Award for Excellence in Clinical Teaching, and the Arthur Bloomfield Award in recognition of excellence in the teaching of clinical medicine.

Clinical Focus


  • Multiple Sclerosis
  • Neuromyelitis Optica
  • Transverse Myelitis
  • Neurology

Academic Appointments


Administrative Appointments


  • Division Chief, Clinical Neuroimmunology (2009 - Present)
  • Director, Stanford Multiple Sclerosis Center & Neuroimmunology Clinic (2008 - Present)
  • Director, Neurology Clerkship Program (2009 - Present)
  • Vice Chair, MS Section, American Academy of Neurology (2014 - Present)
  • Chair, MS Education Workgroup, Multiple Sclerosis Section; American Academy of Neurology (2011 - 2014)
  • Councilor, Executive Committee, Multiple Sclerosis Section; American Academy of Neurology (2010 - 2014)

Honors & Awards


  • Henry J. Kaiser Family Foundation Award for Excellence in Clinical Teaching, Stanford University School of Medicine (2013)
  • Top Doctors, US News & World Report (2012-2013)
  • AUPN Neurology national recuitment award, Association of University Professors of Neurology (2012)
  • Arthur L. Bloomfield Award in Recognition of Excellence in the Teaching of Clinical Medicine, Stanford University School of Medicine (2011)
  • Excellence in Teaching Award, Stanford University School of Medicine (2011-2012)
  • Excellence in Teaching Award, Stanford University School of Medicine (2010-2011)
  • AUPN Neurology Recruitment Award (highest percentage in U.S.), Association of University Professors of Neurology (2011)
  • Excellence in Neurology Clerkship Teaching Award, Stanford University Department of Neurology & Neurosciences (2008,2009,2010,2011,2012,2013)
  • Excellence in Teaching Award, Stanford University School of Medicine (2009-2010)
  • Lysia K. Forno Award for Excellence in Teaching Neurology Residents, Stanford University Department of Neurology & Neurosciences (2008-2009)
  • Fellow, American Academy of Neurology (2008-present)
  • "America's Top Rated Physicians", Guide to Top Doctors (1998-2007, 2010-2013)

Boards, Advisory Committees, Professional Organizations


  • Fellow, American Academy of Neurology (2007 - Present)
  • Member, Consortium of MS Centers (2008 - Present)
  • Member, Accelerated Cure Project (2010 - Present)
  • Member, San Francisco Neurological Society (2009 - Present)

Professional Education


  • Residency:University of Washington Medical Center (1989) WA
  • Internship:Eastern VA Medical School (1989) VA
  • Medical Education:Temple University School of Medicine (1989) PA
  • Board Certification: Neurology, American Board of Psychiatry and Neurology (1994)
  • Residency, University of Washington, Neurology (1993)
  • M.D., Temple University, Medicine (1989)
  • B.A., Haverford College, French Literature (1983)

Community and International Work


  • Editorial Board

    Topic

    Internation Journal of MS Care

    Partnering Organization(s)

    Consortium of MS Centers

    Location

    International

    Ongoing Project

    Yes

    Opportunities for Student Involvement

    No

  • PACTRIMS Member

    Partnering Organization(s)

    Pan Asian Committee for Treatment and Research of Multiple Sclerosis

    Ongoing Project

    Yes

    Opportunities for Student Involvement

    No

Research & Scholarship

Current Research and Scholarly Interests


Translational research in the human application of emerging immunotherapies for neurological disease, focusing on Multiple Sclerosis, CIS, transverse myelitis and Neuromyelitis Optica (NMO). Collaborative research with Stanford and extramural scientific faculty to identify biomarkers of disease activity and treatment response in humans. Clinical trials to assess efficacy of emerging treatments for MS, CIS and NMO.

Clinical Trials


  • An Extension Protocol for Multiple Sclerosis Patients Who Participated in Genzyme-Sponsored Studies of Alemtuzumab Not Recruiting

    This open-label, rater-blinded extension study will enroll patients who have relapsing-remitting multiple sclerosis (RRMS) and who participated in one of three prior Genzyme-sponsored studies of alemtuzumab [CAMMS223 (NCT00050778), CAMMS323 (NCT00530348) also known as CARE-MS I, or CAMMS324 (NCT00548405) also known as CARE-MS II]. The purposes of this study are: 1. To examine the long term safety and efficacy of alemtuzumab treatment in patients who received alemtuzumab as their study treatment in one of the prior studies. 2. To examine the safety and efficacy of initial alemtuzumab treatment in this study for patients who received Rebif® (interferon beta-1a) as their study treatment in one of the prior studies. 3. To determine if and when further alemtuzumab treatment is needed, and the safety and efficacy of this "as needed" treatment. This applies both to patients who received alemtuzumab for the first time in one of the prior studies or for the first time in this extension study.

    Stanford is currently not accepting patients for this trial. For more information, please contact Jeffrey Dunn, MD, 650-736-4310.

    View full details

  • Ponesimod in Patients With Relapsing-remitting Multiple Sclerosis -Extension Study Not Recruiting

    This study is an extension to the study AC-058B201 and will investigate the long-term safety, tolerability and efficacy of ponesimod in patients with relapsing-remitting multiple sclerosis.

    Stanford is currently not accepting patients for this trial. For more information, please contact Angela Campbell, (650) 721-6188.

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  • A Study of Ocrelizumab in Comparison With Interferon Beta-1a (Rebif) in Patients With Relapsing Multiple Sclerosis Not Recruiting

    This randomized, double-blind, double-dummy, parallel-group study will evaluate the efficacy and safety of ocrelizumab in comparison with Rebif (interferon beta-1a) in patients with relapsing multiple sclerosis. Patients will be randomized to receive either in group A, ocrelizumab 600 mg intravenously (iv) every 24 weeks plus Rebif placebo subcutaneously (sc) three times weekly, or, in group B, Rebif 8.8 mcg (Weeks 1+2)/22 mcg (Weeks 3+4)/44 mcg (Week 5 and following) sc three times weekly plus ocrelizumab placebo iv every 24 weeks. Anticipated time on study treatment is 96 weeks.

    Stanford is currently not accepting patients for this trial. For more information, please contact Clinical Trials Office, (650) 498-7061.

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  • Comparison of Alemtuzumab and Rebif® Efficacy in Multiple Sclerosis, Study Two Not Recruiting

    The purpose of this study was to establish the efficacy and safety of two different doses of alemtuzumab (Lemtrada™) as a treatment for relapsing-remitting multiple sclerosis (MS), in comparison with subcutaneous interferon beta-1a (Rebif®). The study enrolled participants who had received an adequate trial of disease-modifying therapies but experienced at least 1 relapse during prior treatment, and who met a minimum severity of disease as measured by magnetic resonance imaging (MRI). Participants had monthly laboratory tests and comprehensive testing every 3 months.

    Stanford is currently not accepting patients for this trial. For more information, please contact Maria Coburn, (650) 736 - 9551.

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  • An Intravenous Infusion Study of rHIgM22 in Patients With Multiple Sclerosis Not Recruiting

    This is a Phase I, multi-center, double-blind, randomized, placebo-controlled, dose-escalation study designed to evaluate safety, tolerability, pharmacokinetics, and immunogenicity of single intravenous (IV) administrations of rHIgM22 in patients with all clinical presentations of MS.

    Stanford is currently not accepting patients for this trial. For more information, please contact Julia Buckingham, (650) 725-7545.

    View full details

Teaching

2014-15 Courses


Publications

All Publications


  • IFN-ß Treatment Requires B Cells for Efficacy in Neuroautoimmunity. Journal of immunology Schubert, R. D., Hu, Y., Kumar, G., Szeto, S., Abraham, P., Winderl, J., Guthridge, J. M., Pardo, G., Dunn, J., Steinman, L., Axtell, R. C. 2015; 194 (5): 2110-2116

    Abstract

    IFN-β remains the most widely prescribed treatment for relapsing remitting multiple sclerosis. Despite widespread use of IFN-β, the therapeutic mechanism is still partially understood. Particularly, the clinical relevance of increased B cell activity during IFN-β treatment is unclear. In this article, we show that IFN-β pushes some B cells into a transitional, regulatory population that is a critical mechanism for therapy. IFN-β treatment increases the absolute number of regulatory CD19(+)CD24(++)CD38(++) transitional B cells in peripheral blood relative to treatment-naive and Copaxone-treated patients. In addition, we found that transitional B cells from both healthy controls and IFN-β-treated MS patients are potent producers of IL-10, and that the capability of IFN-β to induce IL-10 is amplified when B cells are stimulated. Similar changes are seen in mice with experimental autoimmune encephalomyelitis. IFN-β treatment increases transitional and regulatory B cell populations, as well as IL-10 secretion in the spleen. Furthermore, we found that IFN-β increases autoantibody production, implicating humoral immune activation in B cell regulatory responses. Finally, we demonstrate that IFN-β therapy requires immune-regulatory B cells by showing that B cell-deficient mice do not benefit clinically or histopathologically from IFN-β treatment. These results have significant implications for the diagnosis and treatment of relapsing remitting multiple sclerosis.

    View details for DOI 10.4049/jimmunol.1402029

    View details for PubMedID 25646307

  • Mobility Concerns in Multiple Sclerosis US Neurology Lee, J., Dunn, J. 2013; 9 (1): 17-23
  • Disease modifying therapies for non relapsing Multiple Sclerosis Neurol Clin Pract Dunn, J. 2013; December (3): 515-518
  • Randomized study combining interferon and glatiramer acetate in Multiple Sclerosis Annals of Neurology Lublin, F., CombiRx Investigators 2013; 73 (3): 327-340
  • Protective effect of an elastase inhibitor in a neuromyelitis optica-like disease driven by a peptide of myelin oligodendroglial glycoprotein MULTIPLE SCLEROSIS JOURNAL Herges, K., de Jong, B. A., Kolkowitz, I., Dunn, C., Mandelbaum, G., Ko, R. M., Maini, A., Han, M. H., Killestein, J., Polman, C., Goodyear, A. L., Dunn, J., Steinman, L., Axtell, R. C. 2012; 18 (4): 398-408

    Abstract

    The pathology of neuromyelitis optica (NMO), in contrast to multiple sclerosis, comprises granulocyte infiltrates along extensive lengths of spinal cord, as well as optic nerve. Furthermore, IFN-? treatment worsens NMO. We recently found that experimental autoimmune encephalomyelitis (EAE) induced with Th17 cells is exacerbated by IFN-?, in contrast to disease induced with Th1 where treatment attenuated symptoms.This study demonstrates the similarities between NMO and Th17 EAE and how neutrophils mediate pathology in Th17 disease.Levels of blood biomarkers in NMO were assessed by Luminex and ELISA. Effects of IFN-? on neutrophils were assessed by culture assays and immunofluorescence. EAE was induced by transfer of myelin-specific Th1 or Th17 cells and treated with Sivelestat sodium hydrate, a neutrophil elastase inhibitor.We show Th17 cytokines, granulocyte chemokines, type 1 interferon and neutrophil elastase are elevated in patients with definitive NMO. In culture, we find that IFN-? stimulates neutrophils to release neutrophil elastase. In Th17 EAE, we demonstrate neutrophilic infiltration in the optic nerve and spinal cord which was not present in Th1 EAE. Blockade of neutrophil elastase with Sivelestat had efficacy in Th17 EAE but not Th1 EAE.The similarities between Th17 EAE and NMO indicate that this model represents several aspects of NMO. Neutrophils are critical in the pathologies of both Th17-EAE and NMO, and therefore blockade of neutrophil elastase is a promising target in treating NMO.

    View details for DOI 10.1177/1352458512440060

    View details for Web of Science ID 000302289900006

    View details for PubMedID 22343184

  • Protective Effect of elastase inhibitor in a neuromyelitis optica-like disease driven by a peptide of myelin olidodendrocyte glycoprotein Multiple Sclerosis Herges K, DeJong BA, Kolkowitz I, Dunn C, Mandelbaum G, Maini A, Han M, Killestein J, Polman C, Goodyear A, Dunn J, Steinman L, Axtell RC 2012; 18 (4): 398-408
  • Alemtuzumab for patients with relapsing Multiple Sclerosis after disease modifying therapy: a randomized controlled Phase 3 trial. Lancet A, C. J., CARE MS II, I. 2012; Nov 24 (380): 1829-1839
  • Dalfampridine: a brief review of its mechanism of action and efficacy as a treatment to improve walking in patients with multiple sclerosis CURRENT MEDICAL RESEARCH AND OPINION Dunn, J., Blight, A. 2011; 27 (7): 1415-1423

    Abstract

    Multiple sclerosis (MS) can cause progressive walking impairment that contributes to disability, loss of independence, and reduced quality of life. Dalfampridine (4-aminopyridine), a voltage-dependent potassium channel blocker, has been shown to improve walking in patients with MS, as demonstrated by an increase in walking speed.To summarize knowledge about the mechanism of action of dalfampridine in the context of clinical evidence of walking improvement in MS patients.Although this was not a systematic review, which is the primary limitation of this study, searches of PubMed were performed using relevant search terms to identify studies that examined the mechanism of action related to MS and its effects in patients with MS in clinical trials.Voltage-gated potassium channels represent a family of related proteins that span cell membranes, open and close in response to changes in the transmembrane potential, and help regulate ionic potassium currents. Action potential conduction deficits in demyelinated axons result in part from the exposure after demyelination of the paranodal and internodal potassium channels that are distributed in the axonal membrane. This exposure leads to abnormal currents across the axonal membrane that can slow action potential conduction, result in conduction failure, or affect the axon's capacity for repetitive discharge. While dalfampridine is a broad-spectrum blocker of voltage-dependent potassium channels at millimolar concentrations, studies have shown improvement in action potential conduction in demyelinated axons at concentrations as low as 1 ?M, and therapeutic plasma concentrations (associated with improved walking) are in the range of 0.25 µM. However, no specific potassium channel subtype has yet been characterized with significant sensitivity to dalfampridine in this range, and the effects of the drug at this low concentration appear to be quite selective. Improved conduction translates into clinical benefit as measured by objectively and subjectively assessed walking relative to placebo. Such improvements were observed in approximately one third of patients treated with an extended-release formulation of dalfampridine in clinical trials. These patients who responded to dalfampridine had an average increase in walking speed of approximately 25%, and greater improvements than nonresponders on a self-reported subjective measure of walking.The extended-release formulation of dalfampridine has been shown in clinical trials to improve walking speed in approximately one third of MS patients with ambulatory impairment. The putative mechanism of action of dalfampridine is restoration of action potential conduction via blockade of an as yet uncharacterized subset of potassium channels in demyelinated axons.

    View details for DOI 10.1185/03007995.2011.583229

    View details for Web of Science ID 000291662300014

    View details for PubMedID 21595605

  • Dalfampridine: A brief review of its Mechanism of Action and Efficacy as a treatment to improve walking in patients with Multiple Sclerosis Current Research Medical Opinion Dunn J, Blight A 2011; 27 (7): 1415-1423
  • Impact of mobility impairment on the burden of caregiving in individuals with multiple sclerosis EXPERT REVIEW OF PHARMACOECONOMICS & OUTCOMES RESEARCH Dunn, J. 2010; 10 (4): 433-440

    Abstract

    Multiple sclerosis (MS) is a chronic, immune-mediated neurologic disease that typically strikes young adults during their most productive years, and is associated with a wide range of functional deficits and progressive disability. Loss of mobility is among the most disabling effects of MS, adversely affecting multiple outcomes, including independence, employment and quality of life. Relative to other common diseases, MS is associated with a disproportionately high socioeconomic burden. Informal and unpaid caregivers, such as family and friends, play a vital, sustained and often difficult role in supporting the ability of MS patients to live and function at home. However, there are few data characterizing caregiver burden in MS. This review was conducted to examine the need and impact of caregiving for patients with MS, focusing on the contribution of mobility impairment to loss of patient independence.

    View details for DOI 10.1586/ERP.10.34

    View details for Web of Science ID 000297009800017

    View details for PubMedID 20482233

  • Daclizumab in active relapsing multiple sclerosis (CHOICE study): a phase 2, randomised, double-blind, placebo-controlled, add-on trial with interferon beta LANCET NEUROLOGY Wynn, D., Kaufman, M., Montalban, X., Vollmer, T., Simon, J., Elkins, J., O'Neill, G., Neyer, L., Sheridan, J., Wang, C., Fong, A., Rose, J. W. 2010; 9 (4): 381-390

    Abstract

    Daclizumab, a humanised monoclonal antibody, reduced multiple sclerosis disease activity in previous non-randomised studies. We aimed to assess whether daclizumab reduces disease activity in patients with active relapsing multiple sclerosis who are receiving interferon beta treatment.We did a phase 2, randomised, double-blind, placebo-controlled study at 51 centres in the USA, Canada, Germany, Italy, and Spain. Patients with active relapsing multiple sclerosis who were taking interferon beta were randomly assigned to receive add-on subcutaneous daclizumab 2 mg/kg every 2 weeks (interferon beta and high-dose daclizumab group), daclizumab 1 mg/kg every 4 weeks (interferon beta and low-dose daclizumab group), or interferon beta and placebo for 24 weeks. The randomisation scheme was generated by Facet Biotech. All patients and assessors were masked to treatment with the exception of Facet Biotech bioanalysts who prepared data for the data safety monitoring board or generated pharmacokinetic or pharmacodynamic data, a drug accountability auditor, and the site pharmacist. The primary endpoint was total number of new or enlarged gadolinium contrast-enhancing lesions measured on brain MRI scans every 4 weeks between weeks 8 and 24. Effects of daclizumab on prespecified subsets of lymphocytes and quantitative T-cell proliferative response were assessed in an exploratory pharmacodynamic substudy. Analysis was by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT00109161.From May, 2005, to March, 2006, 288 patients were assessed for eligibility, and 230 were randomly assigned to receive interferon beta and high-dose daclizumab (n=75), interferon beta and low-dose daclizumab (n=78), or interferon beta and placebo (n=77). The adjusted mean number of new or enlarged gadolinium contrast-enhancing lesions was 4.75 in the interferon beta and placebo group compared with 1.32 in the interferon beta and high-dose daclizumab group (difference 72%, 95% CI 34% to 88%; p=0.004) and 3.58 in the interferon beta and low-dose daclizumab group (25%, -76% to 68%; p=0.51). In the pharmacodynamic substudy, daclizumab was not associated with significant changes in absolute numbers of T cells, B cells, or natural killer cells, or T-cell proliferative response compared with interferon beta alone. The number of CD56(bright) natural killer cells was seven to eight times higher in both daclizumab groups than in the interferon beta and placebo group (interferon beta and low-dose daclizumab group p=0.002; interferon beta and high-dose daclizumab group p<0.0001). Common adverse events were equally distributed across groups.Add-on daclizumab treatment reduced the number of new or enlarged gadolinium contrast-enhancing lesions compared with interferon beta alone and might reduce multiple sclerosis disease activity to a greater extent than interferon beta alone.Facet Biotech and Biogen Idec.

    View details for DOI 10.1016/S1474-4422(10)70033-8

    View details for Web of Science ID 000276142000016

    View details for PubMedID 20163990

  • The impact of mobility impairment on the burden of caregiving in individuals with multiple sclerosis Expert Rev. Pharmacoeconomics Outcomes Res. Dunn, J. 2010; 10 (4): 433-440
  • Cytomegalovirus Infection with MRI Signal Abnormalities Affecting the Optic Nerves, Optic Chiasm, and Optic Tracts JOURNAL OF NEURO-OPHTHALMOLOGY Pershing, S., Dunn, J., Khan, A., Liao, Y. J. 2009; 29 (3): 223-226

    Abstract

    A 49-year-old woman who had been immunosuppressed after a renal transplant developed bilateral severe visual loss. Visual acuities were finger counting and hand movements in the two eyes. Both optic nerves were pale. There were no other ophthalmic abnormalities. Brain MRI disclosed marked signal abnormalities involving the optic nerves, optic chiasm, and optic tracts. Cerebrospinal fluid polymerase chain reaction (PCR) was positive for cytomegalovirus. Treatment did not restore vision. Such extensive clinical and imaging involvement of the anterior visual pathway, which has been previously reported with other herpes viruses, illustrates the propensity for this family of viruses to track along axons.

    View details for Web of Science ID 000270048700011

    View details for PubMedID 19726946

  • CMV Optic Neuritis with Extensive Tracking along the Visual Pathway J Neuro-Ophthalmology Pershing S, D. K. 2009; 29 (3): 223-226
  • Glatiramer Acetate after Induction Therapy with Mitoxantrone in Relapsing Multiple Sclerosis Multiple Sclerosis Vollmer T, P. B. 2008; Apr 18
  • Tovaxin for Early Relapsing Multiple Sclerosis Phase 2b Placebo Controlled Trial of Autologous T cell vaccination in patients with CIS or RRMS Multiple Sclerosis Fox, E., The TERMS Study Investigators 2008; 14: S5-S27
  • Glatiramer Acetate after Mitoxantrone Induction improves MRI markers of lesion volume and permanent tissue injury in MS J Neurol Arnold D., Campagnolo D., Panitch H., Bar-Or A., Dunn J, Freedman M., Gazda S.K., Vollmer T. 2008; 255: 1473-1478
  • Daclizumab in Patients with Active Relapsing Multiple Sclerosis on Concurrent Interferon beta Therapy; Week 24 data Phase II ECTRIMS Montalban X, K. W. 2007; 10/11/07: S18
  • Randomized, Double Blind, Dose Comparison Study of Glatiramer Acetate in Relapsing Remitting MS Neurology Cohen JA, R. G. 2007; 68 (12): 939-944
  • Safety and Tolerability of Glatiramer Acetate in Pediatric Patients with Relapsing Remitting Multiple Sclerosis ECTRIMS/ACTRIMS Krupp L, Banwell B, Picone M, Dunn J, Weinstock-Guttman B, Pardo L. 2005: abstract
  • Comprehensive Outpatient Management of Patients with Multiple Sclerosis RIMS MS Symposium Odderson I, D. 2001: abstract
  • Novantrone in the Treatment of Multiple Sclerosis Alliance News Dunn Jeffrey, Kita M., Lucas S., Bowen J., 2001: 1-3
  • Clinical Advisory Committee Statement Health Care Connection Bowen J., Dunn Jeffrey E., Kraft G.H., Ratley G., Shilling J., Smith C., Thompson L. 1999; I (1): 1-2
  • Gingko Biloba in the Treatment of Alzheimer's Disease Alternative Medicine Dunn Jeffrey E., Maidan R., Pallis J. 1998; 1 (15): 1-2
  • Atherosclerotic Aortic Disease as a Source of Embolic Infarct Journal of Neurovascular Disease Bursell John P.,Odderson I., Dunn Jeffrey E. 1996; 1 (2): 35-38
  • INTRACEREBRAL BACILLARY ANGIOMATOSIS IN A PATIENT INFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS ANNALS OF INTERNAL MEDICINE Spach, D. H., Panther, L. A., Thorning, D. R., Dunn, J. E., Plorde, J. J., MILLER, R. A. 1992; 116 (9): 740-742

    View details for Web of Science ID A1992HQ62300008

    View details for PubMedID 1558347

  • Intracerebral Bacillary Angiomatosis in a Patient Infected with HIV Annals of Internal Medicine Spach, D., Panther L., Thorning D., Dunn Jeffrey E., Plorde J.L., Miller, R. 1992; 116: 740-743

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