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
Rumble JM, Huber AK, Krishnamoorthy G, Srinivasan A, Giles DA, Zhang X, Wang L, Segal BM. Neutrophil-related factors as biomarkers in EAE and MS. J Exp Med 2015; 212(1):23-35. PMCID: PMC4291533.
Baldwin KT, Carbajal KS, Giger RJ*, Segal BM*. Neuroinflammation triggered by a -glucan/ dectin-1 signaling enables CNS regeneration. Proc Nat Acad Sci 2015; 112(8):2581-6.
PMCID: PMC4345569. *Co-corresponding authors
Phares TW, DiSano KD, Stohlman SA, Segal BM, Bergmann CC. CXCL13 promotes isotype-switched B cell accumulation to the central nervous system during vial encephalomyelitis. Brain Behav Immun. 2016; 54:128-39. PMID: 26795429
Segal BM and Stuve O. Clinical trials in primary progressive multiple sclerosis- why we are Failing. The Lancet. 2016; Epub ahead of print. PMID:26827076
Segal BM and Giger RJ. Stable biomarker for plastic microglia. Proc Nat Acad Sci USA 2016; 113(12):3130-2. PMID: 26966229.
Huber AK, Giles DA, Segal BM, Irani DN. An emerging role of eotaxins in neurodegenerative disease. Clin Immunol. 2016; E pub ahead of print. PMID: 27664933.
Douglas JN, Gardner LA, Salapa HE, Lalor SJ, Lee S, Segal BM, Sawchenko PE, Levin MC. Antibodies to the RNA-binding protein hnRNP A1 contribute to neurodegeneration in a model
of central nervous system autoimmune inflammatory disease. J Neuroinflammation 2016; 13(1):178. PMID: 27391474
Cravens PD, Hussain RZ, Miller-Little WA, Ben L, Segal BM, Herndon E, Stuve O. IL-12/IL-23p40 is highly expressed in secondary lymphoid organs and the CNS during all stages of EAE, but its antagonism does not affect disease perpetuation. PLOS ONE 2016; 11(10):e0165248. PMID: 27780253
Klein RS, Voskuhl R, Segal BM, Dittel BN, Lane TE, et. al. Speaking out about gender imbalance in invited speakers improves diversity. Nat. Immunol. 2017; 18(5):475-478. PMID: 28418385
Neal LM, Xing E, Xu J, Kolbe J, Osterholzer JJ, Segal BM, Williamson PR, Olszewski. CD4+ T cells orchestrate lethal immune pathology despite fungal clearance during Cryptococcus neoformans meningoencephalitis. mBio. 2017. In Press
Duncker PC, Stoolman JS, Huber AK, Segal BM. GM-CSF is dispensable for EAE onset, but drives chronic disability. J. Immunology 2017; In Press
Giles, DA, Washnock-Schmid JM, Duncker OC, Dahlawi S, Ponath G, Pitt D, Segal BM. Myeloid cell plasticity in the evolution of central nervous system autoimmunity. Annals of Neurology. 2018