Dr. Benjamin Matthew Segal M.D.
Neurologist | Neurology
1500 East Medical Center Dr 1st Floor Taubman Ct Ann Arbor MI, 48109Rating
5/5
About
Dr. Benjamin Segal is a distinguished Neurologist in Ann Arbor, MI. Dr. Segal specializes in diagnosing, treating, and managing disorders of the brain and nervous system. With expertise in handling complex conditions like epilepsy, multiple sclerosis, and migraines, Dr. Segal employs advanced techniques and personalized treatment plans to improve patient outcomes. As a neurologist, Dr. Segal is committed to staying abreast of the latest developments in neurological research and therapies.
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Cutting Edge: IL-10-producing CD4+ T cells mediate tumor rejection.
- Activation of APCs through CD40 or Toll-like receptor 9 overcomes tolerance and precipitates autoimmune disease.
- Experimental autoimmune encephalomyelitis: cytokines, effector T cells, and antigen-presenting cells in a prototypical Th1-mediated autoimmune disease.
- IL-12 dependent/IFN gamma independent expression of CCR5 by myelin-reactive T cells correlates with encephalitogenicity.
- Experimental autoimmune encephalomyelitis.
- CNS chemokines, cytokines, and dendritic cells in autoimmune demyelination.
- Cutting edge: IL-12 induces CD4+CD25- T cell activation in the presence of T regulatory cells.
- IL-12 driven upregulation of P-selectin ligand on myelin-specific T cells is a critical step in an animal model of autoimmune demyelination.
- CXC chemokine ligand 13 plays a role in experimental autoimmune encephalomyelitis.
- Th17 and Th1 responses directed against the immunizing epitope, as opposed to secondary epitopes, dominate the autoimmune repertoire during relapses of experimental autoimmune encephalomyelitis.
- Cutting edge: CNS CD11c+ cells from mice with encephalomyelitis polarize Th17 cells and support CD25+CD4+ T cell-mediated immunosuppression, suggesting dual roles in the disease process.
- The role of natural killer cells in curbing neuroinflammation.
- IL-12- and IL-23-modulated T cells induce distinct types of EAE based on histology, CNS chemokine profile, and response to cytokine inhibition.
- Treatment of CNS sarcoidosis with infliximab and mycophenolate mofetil.
- Circulating Ly-6C+ myeloid precursors migrate to the CNS and play a pathogenic role during autoimmune demyelinating disease.
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