Prospects for antigen-specific tolerance based therapies for the treatment of multiple sclerosis.

No abstract is available for this paper.

• Publication year

  2010

• Venue

  Results and problems in cell differentiation

• Publication date

  Unknown publication date

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1007/400_2008_13PMID 19130025PMCID PMC2901403
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• ECDI-fixed allogeneic splenocytes induce donor-specific tolerance for long-term survival of islet transplants via two distinct mechanisms

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• Peripheral Tolerance Induction Using Ethylenecarbodiimide-Fixed APCs Uses both Direct and Indirect Mechanisms of Antigen Presentation for Prevention of Experimental Autoimmune Encephalomyelitis1

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• No effect of oral insulin on residual beta-cell function in recent-onset Type I diabetes (the IMDIAB VII)

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• IL-4, IL-10, IL-13, and TGF-β from an Altered Peptide Ligand-Specific Th2 Cell Clone Down-Regulate Adoptive Transfer of Experimental Autoimmune Encephalomyelitis

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• Tolerance induction to myelin basic protein by intravenous synthetic peptides containing epitope P85 VVHFFKNIVTP96 in chronic progressive multiple sclerosis.

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• Nasal administration of myelin basic protein prevents relapsing experimental autoimmune encephalomyelitis in DA rats by activating regulatory cells expressing IL-4 and TGF-beta mRNA.

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• Predominance of the autoimmune response to myelin oligodendrocyte glycoprotein (MOG) in multiple sclerosis: Reactivity to the extracellular domain of MOG is directed against three main regions

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• Nasal administration of myelin basic protein prevents relapsing experimental autoimmune encephalomyelitis in DA rats by activating regulatory cells expressing IL-4 and TGF-β mRNA

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• A T cell receptor antagonist peptide induces T cells that mediate bystander suppression and prevent autoimmune encephalomyelitis induced with multiple myelin antigens.

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• An important role for the chemokine macrophage inflammatory protein-1 alpha in the pathogenesis of the T cell-mediated autoimmune disease, experimental autoimmune encephalomyelitis.

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• Blockade of CD28/B7-1 interaction prevents epitope spreading and clinical relapses of murine EAE.

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• Copolymer 1 reduces relapse rate and improves disability in relapsing‐remitting multiple sclerosis

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• An altered peptide ligand mediates immune deviation and prevents autoimmune encephalomyelitis.

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• Inhibition of experimental autoimmune encephalomyelitis by inhalation but not oral administration of the encephalitogenic peptide: influence of MHC binding affinity.

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• Epidemiologic evidence for multiple sclerosis as an infection

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• Suppressor T cells generated by oral tolerization to myelin basic protein suppress both in vitro and in vivo immune responses by the release of transforming growth factor beta after antigen-specific triggering.

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• Regulation of the effector stages of experimental autoimmune encephalomyelitis via neuroantigen-specific tolerance induction. II. Fine specificity of effector T cell inhibition.

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• Amelioration of autoimmune encephalomyelitis by myelin basic protein synthetic peptide-induced anergy.

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• Oral tolerance to myelin basic protein and natural recovery from experimental autoimmune encephalomyelitis are associated with downregulation of inflammatory cytokines and differential upregulation of transforming growth factor beta, interleukin 4, and prostaglandin E expression in the brain

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• Prevention of experimental autoimmune encephalomyelitis by antibodies against α4βl integrin

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