about
Temporal pattern of ICAM-I mediated regulatory T cell recruitment to sites of inflammation in adoptive transfer model of multiple sclerosis.Natalizumab-associated PML: Challenges with incidence, resulting risk, and risk stratification.PD-1 regulates neural damage in oligodendroglia-induced inflammation.CD8(+) T-cell pathogenicity in Rasmussen encephalitis elucidated by large-scale T-cell receptor sequencing.Distinct pattern of lesion distribution in multiple sclerosis is associated with different circulating T-helper and helper-like innate lymphoid cell subsets.CD4+NKG2D+ T cells exhibit enhanced migratory and encephalitogenic properties in neuroinflammation.Assessment of immune functions and MRI disease activity in relapsing-remitting multiple sclerosis patients switching from natalizumab to fingolimod (ToFingo-Successor).Impaired NK-mediated regulation of T-cell activity in multiple sclerosis is reconstituted by IL-2 receptor modulationB7-H1 shapes T-cell-mediated brain endothelial cell dysfunction and regional encephalitogenicity in spontaneous CNS autoimmunity.Janus head: the dual role of HLA-G in CNS immunity.Therapeutic uses of anti-α4-integrin (anti-VLA-4) antibodies in multiple sclerosis.Single-cell profiling reveals GPCR heterogeneity and functional patterning during neuroinflammation.Anti-JCV serology during natalizumab treatment: Review and meta-analysis of 17 independent patient cohorts analyzing anti-John Cunningham polyoma virus sero-conversion rates under natalizumab treatment and differences between technical and biologicaMelanocortin-1 receptor activation is neuroprotective in mouse models of neuroinflammatory disease.Therapy with natalizumab is associated with high JCV seroconversion and rising JCV index values.Liver X receptor activation promotes differentiation of regulatory T cells.VLA-4 blockade promotes differential routes into human CNS involving PSGL-1 rolling of T cells and MCAM-adhesion of TH17 cells.Accelerated course of experimental autoimmune encephalomyelitis in PD-1-deficient central nervous system myelin mutants.Specific loss of cellular L-selectin on CD4(+) T cells is associated with progressive multifocal leukoencephalopathy development during HIV infection.CD8+ T-cell clones dominate brain infiltrates in Rasmussen encephalitis and persist in the periphery.Trafficking of lymphocytes into the CNS.Ultraviolet B light attenuates the systemic immune response in central nervous system autoimmunity.FOXP3+ T regulatory cells in idiopathic inflammatory myopathies.CD8+ T-cell immunity in chronic inflammatory demyelinating polyradiculoneuropathy.Early detrimental T-cell effects in experimental cerebral ischemia are neither related to adaptive immunity nor thrombus formation.Nitazoxanide May Modify the Course of Progressive Multifocal Leukoencephalopathy.Dual action by fumaric acid esters synergistically reduces adhesion to human endothelium.L-selectin is a possible biomarker for individual PML risk in natalizumab-treated MS patients.T cell suppression by naturally occurring HLA-G-expressing regulatory CD4+ T cells is IL-10-dependent and reversible.Chemokine CCL17 is expressed by dendritic cells in the CNS during experimental autoimmune encephalomyelitis and promotes pathogenesis of disease.Immunological and clinical consequences of treating a patient with natalizumab.PML risk stratification using anti-JCV antibody index and L-selectin.Sex bias in MHC I-associated shaping of the adaptive immune system.Analysis of Lymphocyte Extravasation Using an In Vitro Model of the Human Blood-brain Barrier.Intercellular exchanges of membrane fragments (trogocytosis) between human muscle cells and immune cells: a potential mechanism for the modulation of muscular immune responses.CD62L test at 2 years of natalizumab predicts progressive multifocal leukoencephalopathy.Blockade of MCAM/CD146 impedes CNS infiltration of T cells over the choroid plexusHuman myoblasts modulate the function of antigen-presenting cellsDietary salt promotes ischemic brain injury and is associated with parenchymal migrasome formationDoes the environment influence multiple sclerosis pathogenesis via UVB light and/or induction of vitamin D?
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Nicholas Schwab
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Nicholas Schwab
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Nicholas Schwab
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Nicholas Schwab
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Nicholas Schwab
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Nicholas Schwab
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Nicholas Schwab
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Nicholas Schwab
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Nicholas Schwab
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Nicholas Schwab
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Nicholas Schwab
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Nicholas Schwab
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Nicholas Schwab
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Nicholas Schwab
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