Encephalomyelitis, Autoimmune, Experimental
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Subject Areas on Research
- A comparative analysis of multiple sclerosis-relevant anti-inflammatory properties of ethyl pyruvate and dimethyl fumarate.
- A validated regulatory network for Th17 cell specification.
- Accelerated induction of experimental allergic encephalomyelitis in PL/J mice by a non-V beta 8-specific superantigen.
- An interferon-β-resistant and NLRP3 inflammasome-independent subtype of EAE with neuronal damage.
- Apolipoprotein E-derived peptides ameliorate clinical disability and inflammatory infiltrates into the spinal cord in a murine model of multiple sclerosis.
- Association between cell-mediated demyelination and astrocyte stimulation.
- Bone marrow-derived dendritic cells pulsed with tumor homogenate induce immunity against syngeneic intracerebral glioma.
- Circulating adhesion molecules and inflammatory mediators in demyelination: a review.
- Cytosolic phospholipase A2 alpha-deficient mice are resistant to experimental autoimmune encephalomyelitis.
- EAE cerebrospinal fluid augments in vitro phagocytosis and metabolism of CNS myelin by macrophages.
- Engagement of the type I interferon receptor on dendritic cells inhibits T helper 17 cell development: role of intracellular osteopontin.
- Experimental allergic encephalomyelitis in Lewis rats bearing avian sarcoma virus-induced brain tumors.
- Experimental autoimmune encephalomyelitis in mice lacking glial fibrillary acidic protein is characterized by a more severe clinical course and an infiltrative central nervous system lesion.
- G protein-coupled receptor kinase 2 in multiple sclerosis and experimental autoimmune encephalomyelitis.
- Genetic deficiency of Irgm1 (LRG-47) suppresses induction of experimental autoimmune encephalomyelitis by promoting apoptosis of activated CD4+ T cells.
- Hyperimmunization of non-human primates with BCG-CW and cultured human glioma-derived cells. Production of reactive antisera and absence of EAE induction.
- Imaging inflammation: direct visualization of perivascular cuffing in EAE by magnetic resonance microscopy.
- Immunomodulation of experimental autoimmune encephalomyelitis by helminth ova immunization.
- Immunoregulation of CNS autoimmunity by helminth and mycobacterial infections.
- Induction of anti-myelin antibodies in EAE and their possible role in demyelination.
- Induction of lethal experimental allergic encephalomyelitis in nonhuman primates and guinea pigs with human glioblastoma multiforme tissue.
- 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.
- Inflammasome activation in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE).
- Inhibitory role of CD19 in the progression of experimental autoimmune encephalomyelitis by regulating cytokine response.
- Interferon-β therapy against EAE is effective only when development of the disease depends on the NLRP3 inflammasome.
- Intrinsic and induced regulation of the age-associated onset of spontaneous experimental autoimmune encephalomyelitis.
- Introduction: Regulatory B Cell Special Issue-making all the pieces fit.
- Leptin directly promotes T-cell glycolytic metabolism to drive effector T-cell differentiation in a mouse model of autoimmunity.
- Lung inflammation stalls Th17-cell migration en route to the central nervous system during the development of experimental autoimmune encephalomyelitis.
- Marking and quantifying IL-17A-producing cells in vivo.
- Metabolic programming and PDHK1 control CD4+ T cell subsets and inflammation.
- MicroRNA-31 negatively regulates peripherally derived regulatory T-cell generation by repressing retinoic acid-inducible protein 3.
- Microparticles bearing encephalitogenic peptides induce T-cell tolerance and ameliorate experimental autoimmune encephalomyelitis.
- Mnk1 and 2 are dispensable for T cell development and activation but important for the pathogenesis of experimental autoimmune encephalomyelitis.
- NLRP3 inflammasome induces chemotactic immune cell migration to the CNS in experimental autoimmune encephalomyelitis.
- Neurotoxin quinolinic acid is selectively elevated in spinal cords of rats with experimental allergic encephalomyelitis.
- PD-1/PD-L1, but not PD-1/PD-L2, interactions regulate the severity of experimental autoimmune encephalomyelitis.
- Purkinje cell loss in 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.
- Regulatory B cells control T-cell autoimmunity through IL-21-dependent cognate interactions.
- Regulatory B cells inhibit EAE initiation in mice while other B cells promote disease progression.
- Short-term sPECAM-Fc treatment ameliorates EAE while chronic use hastens onset of symptoms.
- Systemic CTLA-4 blockade ameliorates glioma-induced changes to the CD4+ T cell compartment without affecting regulatory T-cell function.
- T-bet-dependent expression of osteopontin contributes to T cell polarization.
- TGF-beta-induced myelin peptide-specific regulatory T cells mediate antigen-specific suppression of induction of experimental autoimmune encephalomyelitis.
- The IFN pregnancy recognition hormone IFN-tau blocks both development and superantigen reactivation of experimental allergic encephalomyelitis without associated toxicity.
- The oligodendrocyte-specific G protein-coupled receptor GPR17 is a cell-intrinsic timer of myelination.
- The role of interferon-β in the treatment of multiple sclerosis and experimental autoimmune encephalomyelitis - in the perspective of inflammasomes.
- Tolerance induced by apoptotic antigen-coupled leukocytes is induced by PD-L1+ and IL-10-producing splenic macrophages and maintained by T regulatory cells.
- Transcriptional regulator Id2 is required for the CD4 T cell immune response in the development of experimental autoimmune encephalomyelitis.
- miR-17-92 cluster targets phosphatase and tensin homology and Ikaros Family Zinc Finger 4 to promote TH17-mediated inflammation.
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Keywords of People
- Ciofani, Maria, Assistant Professor of Immunology, Immunology
- Gunn, Michael Dee, Professor of Medicine, Immunology
- McLendon, Roger Edwin, Professor of Pathology, Pathology
- Sampson, John Howard, Robert H., M.D. and Gloria Wilkins Professor of Neurosurgery, in the School of Medicine, Immunology
- Shinohara, Mari L., Associate Professor of Immunology, Immunology