MAR 19, 2014 07:00 AM PDT

A Unique B Cell Derived Signature of Multiple Sclerosis and its Biologic Implications

Presented At Neuroscience
  • Associate Professor Cain Denius Scholar in Mobility Disorders, Department of Neurology & Neurotherapeutics, Pediatrics, UT Southwestern Medical Center
      Dr. Benjamin Greenberg received his Bachelor of Arts degree from Johns Hopkins University and his Masters Degree in Molecular Microbiology and Immunology from the Johns Hopkins School of Public Health in Baltimore, Maryland. He attended medical school at Baylor College of Medicine in Houston, Texas. Then, he completed an internship in medicine at Rush Presbyterian-St. Luke?s Medical Center in Chicago, Illinois before going on to his residency in neurology at The Johns Hopkins Hospital in Baltimore, MD. He then joined the faculty within the division of neuroimmunology at Hopkins and became the co-director of the Transverse Myelitis Center and director of the Encephalitis Center. In January of 2009 he was recruited to the faculty at the University of Texas Southwestern Medical Center where he was named Deputy Director of the Multiple Sclerosis Program and Director of the new Transverse Myelitis and Neuromyelitis Optica Program. His research interests are in both the diagnosis and treatment of multiple sclerosis, transverse myelitis, neuromyelitis optica and infections of the nervous system. He is actively involved in developing better ways to diagnose and prognosticate for patients with these disorders. He has led an effort to improve biorepository development and has created uniform protocols for sample handling and analysis. As part of this initiative his research has identified novel biomarkers that may be able to distinguish between patients with various neurologic disorders. He also coordinates trials that study new treatments to prevent neurologic damage and restore function to those who have already been affected.


    Multiple Sclerosis (MS) is an autoimmune disease that leads to widespread pathology within the central nervous system (CNS) and is the most common cause of neurologic disability among young adults within the US. Pathologic descriptions of multiples sclerosis have documented damage to the myelin sheath around axons and to underlying neurons. The mechanism of damage has long been ascribed to auto reactive T cells that infiltrate the CNS and cause tissue injury. Over the last decade, however, a significant amount of data has implicated a deranged B cell biology in the pathogenesis of this disabling condition. Work completed within labs at UT Southwestern have identified a novel pattern of somatic hypermutation among B cells from MS patients. This pattern is currently being studied as a potential new biomarker or diagnostic test for the condition. Continued research has begun to determine the antigenic targets of this deranged B cell biology and will point the field in new research directions. This presentation will present data relative to the identified pattern of somatic hypermutation from MS patients, the biology of the produced antibodies from these unique cells and implications for future research.

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