Subject Areas on Research
- Anti-Myelin Oligodendrocyte Glycoprotein Optic Neuritis or Neuroretinitis?
- Clinical Reasoning: An 11-year-old girl with focal seizures, fevers, and unilateral, enhancing cortical lesions.
- Cytosolic phospholipase A2 alpha-deficient mice are resistant to experimental autoimmune encephalomyelitis.
- Dectin-1 limits autoimmune neuroinflammation and promotes myeloid cell-astrocyte crosstalk via Card9-independent expression of Oncostatin M.
- Degenerate TCR recognition and dual DR2 restriction of autoreactive T cells: implications for the initiation of the autoimmune response in multiple sclerosis.
- Estrogen receptor-β ligand treatment after disease onset is neuroprotective in the multiple sclerosis model.
- Infection with Mycobacterium bovis BCG diverts traffic of myelin oligodendroglial glycoprotein autoantigen-specific T cells away from the central nervous system and ameliorates experimental autoimmune encephalomyelitis.
- Inhibitory role of CD19 in the progression of experimental autoimmune encephalomyelitis by regulating cytokine response.
- Linkage analysis of candidate myelin genes in familial multiple sclerosis.
- Mnk1 and 2 are dispensable for T cell development and activation but important for the pathogenesis of experimental autoimmune encephalomyelitis.
- Neuromyelitis optica spectrum disorder and myelin oligodendrocyte glycoprotein associated disorder-optic neuritis: a comprehensive review of diagnosis and treatment.
- PD-1/PD-L1, but not PD-1/PD-L2, interactions regulate the severity of experimental autoimmune encephalomyelitis.
- Regulatory B cells (B10 cells) and regulatory T cells have independent roles in controlling experimental autoimmune encephalomyelitis initiation and late-phase immunopathogenesis.
- Substance P receptor mediated maintenance of chronic inflammation in EAE.
- TGF-beta-induced myelin peptide-specific regulatory T cells mediate antigen-specific suppression of induction of experimental autoimmune encephalomyelitis.
- The clinical presentation and treatment of MOG antibody disease at a single academic center: A case series.
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