about
Stage-specific immune dysregulation in multiple sclerosisTreatment of CNS sarcoidosis with infliximab and mycophenolate mofetilThe critical role of IL-12 and the IL-12R beta 2 subunit in the generation of pathogenic autoreactive Th1 cells.GM-CSF-dependent, CD103+ dermal dendritic cells play a critical role in Th effector cell differentiation after subcutaneous immunization.Th17 cells in autoimmune demyelinating disease.Site-specific chemokine expression regulates central nervous system inflammation and determines clinical phenotype in autoimmune encephalomyelitisDysregulation of the IL-23/IL-17 axis and myeloid factors in secondary progressive MS.Neutrophil-related factors as biomarkers in EAE and MS.Neuroinflammation triggered by β-glucan/dectin-1 signaling enables CNS axon regeneration.Th Cell Diversity in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis.An interleukin (IL)-10/IL-12 immunoregulatory circuit controls susceptibility to autoimmune disease.The role of natural killer cells in curbing neuroinflammationThe Th17-ELR+ CXC chemokine pathway is essential for the development of central nervous system autoimmune diseaseIL-12- and IL-23-modulated T cells induce distinct types of EAE based on histology, CNS chemokine profile, and response to cytokine inhibition.Stable biomarker for plastic microgliaCXCL13 promotes isotype-switched B cell accumulation to the central nervous system during viral encephalomyelitis.Virus-induced CD8+ T cells accelerate the onset of experimental autoimmune encephalomyelitis: implications for how viral infections might trigger multiple sclerosis exacerbations.Notch signaling regulates T cell accumulation and function in the central nervous system during experimental autoimmune encephalomyelitis.Antibodies to the RNA-binding protein hnRNP A1 contribute to neurodegeneration in a model of central nervous system autoimmune inflammatory disease.Circulating Ly-6C+ myeloid precursors migrate to the CNS and play a pathogenic role during autoimmune demyelinating disease.The unwavering commitment of regulatory T cells in the suppression of autoimmune encephalomyelitis: another aspect of immune privilege in the CNSHighly polarized Th17 cells induce EAE via a T-bet independent mechanism.Obstructive sleep apnea and fatigue in patients with multiple sclerosis.T(H)17 cytokines in autoimmune neuro-inflammation.Neurosarcoidosis: diagnostic approaches and therapeutic strategies.The dual roles of immunity in ALS: injury overrides protection.An emerging role for eotaxins in neurodegenerative disease.B-cell targeting agents in the treatment of multiple sclerosis.T-bet promotes the accumulation of encephalitogenic Th17 cells in the CNS.IL-12-polarized Th1 cells produce GM-CSF and induce EAE independent of IL-23.Hypnotic use and fatigue in multiple sclerosis.Getting to the crux of the matter: IL-23 and Th17 cell accumulation in the CNS.Obstructive sleep apnea is an under-recognized and consequential morbidity in multiple sclerosis.Underrecognition of sleep disorders in patients with multiple sclerosis.CD4+ T Cells Orchestrate Lethal Immune Pathology despite Fungal Clearance during Cryptococcus neoformans Meningoencephalitis.GM-CSF Promotes Chronic Disability in Experimental Autoimmune Encephalomyelitis by Altering the Composition of Central Nervous System-Infiltrating Cells, but Is Dispensable for Disease Induction.Myeloid cell plasticity in the evolution of central nervous system autoimmunity.The straight talk on immune deviation.Th1-mediated experimental autoimmune encephalomyelitis is CXCR3 independent.Th17 and Th1 responses directed against the immunizing epitope, as opposed to secondary epitopes, dominate the autoimmune repertoire during relapses of experimental autoimmune encephalomyelitis.
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hulumtues
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Benjamin M. Segal
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Benjamin M. Segal
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Benjamin M. Segal
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Benjamin M. Segal
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Benjamin M. Segal
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Benjamin M. Segal
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Benjamin M. Segal
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Benjamin M. Segal
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Benjamin M. Segal
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Benjamin M. Segal
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Benjamin M. Segal
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Benjamin M. Segal
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Benjamin M. Segal
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7102467628
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P496
0000-0002-0906-6319