Benjamin Segal, M.D.
Affiliations: | Immunology | University of Michigan, Ann Arbor, Ann Arbor, MI |
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"Benjamin Segal"Mean distance: 31.11 (cluster 11)
Cross-listing: Chemistry Tree
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Sign in to add trainee| Patrick Duncker | grad student | 2018 | University of Michigan |
| Jeffrey R Atkinson | post-doc | 2018- | Ohio State University Wexner Medical Center |
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Publications
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| Mockus TE, Munie A, Atkinson JR, et al. (2021) Encephalitogenic and Regulatory CD8 T Cells in Multiple Sclerosis and Its Animal Models. Journal of Immunology (Baltimore, Md. : 1950). 206: 3-10 |
| Kalinski AL, Yoon C, Huffman LD, et al. (2020) Analysis of the immune response to sciatic nerve injury identifies efferocytosis as a key mechanism of nerve debridement. Elife. 9 |
| Sas AR, Carbajal KS, Jerome AD, et al. (2020) A new neutrophil subset promotes CNS neuron survival and axon regeneration. Nature Immunology |
| Douglas JN, Gardner LA, Salapa HE, et al. (2016) Antibodies to the RNA-binding protein hnRNP A1 contribute to neurodegeneration in a model of central nervous system autoimmune inflammatory disease. Journal of Neuroinflammation. 13: 178 |
| Segal BM, Giger RJ. (2016) Stable biomarker for plastic microglia. Proceedings of the National Academy of Sciences of the United States of America |
| Phares TW, DiSano KD, Stohlman SA, et al. (2016) CXCL13 promotes isotype-switched B cell accumulation to the central nervous system during viral encephalomyelitis. Brain, Behavior, and Immunity |
| Carbajal KS, Mironova Y, Ulrich-Lewis JT, et al. (2015) Th Cell Diversity in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis. Journal of Immunology (Baltimore, Md. : 1950). 195: 2552-9 |
| Grifka-Walk HM, Giles DA, Segal BM. (2015) IL-12-polarized Th1 cells produce GM-CSF and induce EAE independent of IL-23. European Journal of Immunology. 45: 2780-6 |
| Murdock BJ, Bender DE, Segal BM, et al. (2015) The dual roles of immunity in ALS: injury overrides protection. Neurobiology of Disease. 77: 1-12 |
| Baldwin KT, Carbajal KS, Segal BM, et al. (2015) Neuroinflammation triggered by β-glucan/dectin-1 signaling enables CNS axon regeneration. Proceedings of the National Academy of Sciences of the United States of America. 112: 2581-6 |