Benjamin Segal, M.D.
As the Holtom-Garrett Professor of Neurology, Dr. Segal directs the University of Michigan Multiple Sclerosis Center and Program in Neuroimmunology. He also serve as Chair of the Scientific Advisory Board, VA Multiple Sclerosis Centers of Excellence-East and is co-Chair of the Americas Committee on Research and Teaching in MS (ACTRIMS) planning committee. The UM MS Center provides multidisciplinary care for over 3,300 patients with MS. The Center is engaged in numerous trials of novel drugs and procedures for the treatment of relapsing-remitting and progressive forms of MS. In addition, Dr. Segal oversees a basic laboratory program in which animal models are used to elucidate the roles of leukocyte subsets, and cytokine and chemokine pathways, in CNS pathology as well as regeneration.
Research efforts in the Segal laboratory span preclinical, translational, and clinical studies in neuroimmunological disease. The laboratory investigates the role of cytokine and chemokines, and the interplay between the acquired and innate immune systems, in animal models of neuroinflammation as well as in subjects with MS and related disorders. Strategies to exploit the "protective" aspects of the immune system to promote nerve fiber regeneration and remyelination are also under investigation.
Research Opportunities for Rotating Students
- Immune mediated axonal regeneration
- Role of myelin associated inhibitors in the immune response
- Myeloid cells and related factors in Multiple Sclerosis and its animal models
Lalor S and Segal BM. TH1 mediated experimental autoimmune encephalomyelitis in CXCR3-independent. Eur. J. Immunol.; In Press
Rainey-Barger EK, Blakely PK, Huber AK, Segal BM and Irani DN. Virus-induced CD8+ T cells accelerate the onset of experimental autoimmune encephalomyelitis: implications for how viral infections might trigger multiple sclerosis exacerbations. J Neuroimmunol. 2013; In Press. PMCID: PMC3654028
Sandy AR, Stoolman J, Mallot K, Pangtornpipat P, Segal BM and Maillard I. Notch signaling regulates T cell accumulation and function in the central nervous system during experimental autoimmune encephalomyelitis. J Immunol 2013; 191(4):1606-1613. PMCID: PMC3735619.
Lalor SJ, Segal BM. Th1-mediated experimental autoimmune encephalomyelitis is CXCR3 independent. Eur J Immunol 2013; 43(11):2866-74. PMID: 23873018
Grifka-Walk HM, Lalor SJ, and Segal BM. Highly polarized Th17 cells induce EAE via a T-bet independent mechanism. Eur. J. Immunol 2013 Nov; 43(11):2824-2831. PMCID: PMC3838449.
Braley TJ, Segal BM, and Chervin RD. Obstructive sleep apnea and fatigue in patients with multiple sclerosis. J Clin Sleep Med 2014;10(2):155-162. PMCID: PMC3899317.
Segal BM. Stage Specific Immune Dysregulation in Multiple Sclerosis. Journal of Interferon & Cytokine Research 2014 (In Press).
Rumble J and Segal BM. In Vitro Polarization of Th cells. In “T-Helper Cells: Methods and Protocols” (A. Waisman and B. Becher, ed.s) 2014 (In Press).
Stoolman JS, Duncker PC, Huber AK and Segal BM. Site-specific chemokine expression regulates CNS inflammation and determines clinical phenotype in autoimmune encephalomyelitis. J Immunol 2014; PMCID: PMC409164.
Braley TJ, Segal BM, Chervin RD. Obstructive sleep apnea is an under-recognized and consequently morbidity in multiple sclerosis. J Clin Sleep Med 2014; 10(6):709-10. PMCID: PMC4031420