Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A panel of myelin basic protein (MBP)-specific, class II major histocompatibility complex (As)-restricted T-cell clones were established from SJL/J mice. Three clonotypes, based on their responses to guinea pig MBP and its peptide fragments, were observed. Clonotype I cells, represented by clones HS.6, HS.D2, HS.8, HS.E10, and HS.C1, were reactive to the encephalitogenic C-terminal fragment of MBP, amino acid residues 89-169. Clonotype II, represented by clone HS.E3, was reactive to fragments containing residues 43-88, and clones HS.D12 and HS.C7, representing clonotype III cells, responded to the whole molecule only. Three clones from clonotype I were capable of transferring both clinical and histological signs of experimental allergic encephalomyelitis (EAE) into naive mice. Southern blot analysis of T-cell receptor beta-chain genes using J beta 1- and J beta 2-specific probes showed that the rearrangement pattern was unique in each of the clones. These results suggest that the development of EAE may represent an autoaggressive polyclonal T-cell response.
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PMID:Clonal diversity of myelin basic protein-specific T lymphocytes. 245 38

Light and electron immunocytochemistry using antibodies recognising a class II major histocompatibility complex antigen, fibrin, fibronectin, albumin and factor VIII related antigen has been used to stain sections of spinal cord from normal guinea pigs and those with chronic relapsing experimental allergic encephalomyelitis (CREAE). It was found that class II MHC antigens, fibrin and fibronectin were present in normal blood vessels and at high levels in lesions from animals at all stages of the disease. The possible immunological roles of these antigens suggest their participation in the initiation and maintenance of disease state.
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PMID:The localisation of fibrin, fibronectin and class II major histocompatibility complex antigen in the spinal cord in chronic relapsing experimental allergic encephalomyelitis. 246 10

Cellular immune reactions against the autoantigen myelin basic protein (MBP) are strongly implicated in the occurrence of postinfectious and postvaccination encephalomyelitis. Clinical autoimmune encephalomyelitis in experimental animals can be transferred with cloned MBP-specific cytolytic major histocompatibility complex Class II-restricted T lymphocytes. The HLA restriction pattern of specific proliferative and cytolytic functions of two human MBP-specific cytotoxic T lymphocyte clones, derived from two different multiple sclerosis patients, was analyzed in detail. Using monoclonal antibodies against various HLA gene products and allogeneic Epstein-Barr virus-transformed B cells as antigen-presenting cells and as targets for cytolysis, it was found that MBP-specific functions of the T cell clones was restricted by HLA class II antigens, and, more specifically, by molecules encoded for by DR locus genes.
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PMID:Human myelin basic protein-specific cytolytic T lymphocyte clones are functionally restricted by HLA class II gene products. 246 52

Myelin basic protein (MBP)-specific T cell lines and clones have been established from rats of the major histocompatibility complex (MHC)-compatible Lewis and BS strains. All lines and clones are MHC class II restricted and share the CD4+ phenotype. The cells proliferate specifically in response to either a peptide representing amino acids #68-88 of guinea pig MBP, to residues #47-67 or to an unidentified myelin antigen which is distinct from MBP. All lines and clones specific for MBP express the same T cell receptor (TcR) variable (V) beta chain element, which is homologous to the mouse V beta 8.2 gene segment. Three lines/clones with the same antigen fine specificity have identical V beta D beta J beta junctions on the protein level, a region which represents part of the potential antigen-binding portion of the TcR; two of the lines express members of the V alpha 2 family. These results suggest biased usage of TcR V beta elements in rat T cells specific for MBP. Our findings broaden the basis for a rational therapeutic strategy to specifically intervene in the rodent model system of experimental allergic encephalomyelitis.
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PMID:T cell receptor beta chain usage in myelin basic protein-specific rat T lymphocytes. 246 13

Two synthetic immunodominant and nonencephalitogenic peptides of myelin basic protein, N1-20 and AcN9-20, effectively compete with an encephalitogenic peptide, AcN1-11, in an in vitro T-cell response restricted by class II major histocompatibility complex products (I-Au). These mutant peptide constructs, which do not occur in nature, also compete with the self-antigen for the in vivo induction of T cells primed with the encephalitogen AcN1-11. By using these nonpathogenic competitor peptides, it is possible to prevent the development of a prototypic T-cell-mediated autoimmune disease, experimental allergic encephalomyelitis. These results suggest possibilities for the utilization of competitor peptides for therapy of T-cell-mediated autoimmune diseases linked to specific major histocompatibility complex genes.
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PMID:Prevention of experimental encephalomyelitis with peptides that block interaction of T cells with major histocompatibility complex proteins. 248 Jun 2

Multiple sclerosis is a demyelinating disease of the central nervous system with genetic, viral and autoimmune characteristics. Myelin basic protein (MBP) is a suspected target autoantigen since it induces experimental autoimmune encephalomyelitis, an animal model closely resembling multiple sclerosis. The disease is mediated by Class II restricted, MBP-reactive T cells possessing the T helper/inducer phenotype. In the present study, we have isolated MBP-reactive T cell clones from the peripheral blood of a chronic progressive multiple sclerosis patient. The clones displayed blastogenic memory responses when rechallenged with the autoantigen and irradiated autologous lymphocytes. MBP recognition by the autoantigen-reactive T lymphocytes was restricted by major histocompatibility complex Class II antigens. Both CD4+8- and CD4-8+ MBP-reactive T cell clones were obtained.
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PMID:MHC-restricted autoantigen-reactive T cell clones in multiple sclerosis. 248 13

We prepared RNA probes from cloned segments of human and murine enteroviruses (EVs) for in situ hybridization of skeletal muscle biopsies from patients with dermatomyositis (DM), polymyositis, other inflammatory myopathies, and noninflammatory muscle diseases, and from normal control subjects. A probe derived from Theiler's murine encephalomyelitis virus (TMEV) detected viral RNA within mononuclear cells of the interstitial connective tissue in 3 of 5 patients with adult-onset DM. None of these patients showed positive hybridization to probes derived from human EVs (poliovirus type 1 and Coxsackie virus B3) applied to subjacent sections of the same biopsies. The remaining 2 adult DM patients, 4 patients with childhood-onset DM, and 24 non-DM patients did not react with either TMEV or human enterovirus probes. Histochemical stains for esterase and immunoperoxidase stains for Mac-1 antigen in the 3 DM patients who reacted positively revealed positive cells in the same distribution as, but in far greater number than, those positive by in situ hybridization. Immunoperoxidase staining for HLA-DR antigens revealed positive cells in the same distribution and number as were seen with the TMEV probe. We conclude that an EV-like agent, more closely related to TMEV than to human EVs, may be associated with DM and that this agent is probably localized within muscle macrophages that express class II major histocompatibility complex antigens.
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PMID:Evidence for a novel picornavirus in human dermatomyositis. 254 50

This study was undertaken to determine if there is differential expression of the relevant strain-specific Ia antigen on endothelial and parenchymal inflammatory cells in the central nervous systems (CNS) of guinea pigs (GP) with acute experimental allergic encephalomyelitis (EAE). Adult inbred GP were sensitized with GP spinal cord homogenate and complete Freund's adjuvant. Strain 13 GP and (2 x 13)F1 hybrids developed clinical disease within 2 to 3 wk after sensitization, whereas strain 2 GP did not, although all sensitized GP had CNS mononuclear inflammatory infiltrates. By using monoclonal antibodies to strain-specific and framework Ia epitopes with an immunoperoxidase technique, the distribution and amount of the strain 2 and strain 13 Ia were analyzed. Equivalent strain 2 and strain 13 Ia expression was found in normal tissues from F1 animals. Strain 2 and strain 13 GP sensitized for EAE had increased strain-specific Ia staining of CNS vessels and inflammatory cells over controls. However, F1 GP with EAE had markedly increased strain 13, but not strain 2, Ia on CNS parenchymal vessels and mononuclear inflammatory cells (p less than 0.001, for both). These results suggest for the first time that specific major histocompatibility complex gene products are selectively expressed on endothelial and inflammatory cells in situ in immune reactions in the target organ of individuals of heterogeneous immunogenetic composition.
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PMID:The immunopathology of experimental allergic encephalomyelitis (EAE). III. Differential in situ expression of strain 13 Ia on endothelial and inflammatory cells of (strain 2 x strain 13)F1 guinea pigs with EAE. 257 41

Previous studies have shown that vascular endothelial cells do not normally express major histocompatibility complex (MHC) Class II antigens either in vivo or in vitro. In this investigation it was found that endothelial in the central nervous system (CNS) of normal guinea pigs constitutively express MHC Class II antigens recognized by the monoclonal antibodies HLA-DR, 27E7, and MSgp8. This phenotype is retained when these CNS-derived endothelial cells are propagated in tissue culture. Furthermore, examination of CNS tissue taken from animals in the acute phase of chronic relapsing experimental allergic encephalomyelitis shows that additional epitopes of the MHC Class II antigen, detected by the monoclonal antibodies CI.13.1 and 22C4, are present during the diseased state. This study not only demonstrates constitutive expression of certain MHC Class II determinants by guinea pig endothelial cells, but also shows that other Class II determinants can be differentially expressed in certain disease states.
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PMID:Differential expression of guinea pig class II major histocompatibility complex antigens on vascular endothelial cells in vitro and in experimental allergic encephalomyelitis. 264 58

T-lymphocytes recognize antigen in a trimolecular complex: The T-cell receptor binds to a processed fragment of antigen that itself is bound to a major histocompatibility complex (MHC) molecule on the surface of an antigen-presenting cell. The trimolecular complex controls antigen-specific T-cell activation in normal and abnormal immune reactions. Recent progress in myasthenia gravis (MG) and experimental autoimmune encephalomyelitis (EAE) exemplifies this, leading to the following conclusions: (1) Autoimmune T cells may act by interfering with immunoregulation (as in MG) or by directly mediating autoimmune damage (as in EAE), or both. (2) In both diseases, the autoimmune T cells are clonally heterogeneous but recognize only a limited number of epitopes on the autoantigen (acetylcholine receptor in MG; myelin basic protein in EAE). Many of these epitopes can be defined as short peptide fragments of antigen, bound to a particular type of MHC molecule. (3) The MHC determines which peptides are recognized by autoimmune T cells in a given patient or inbred animal strain. (4) The discovery of the limited repertoire of autoimmune T cells has allowed considerable progress in the immunotherapy of EAE, using either monoclonal antibodies or cytotoxic T cells directed against clonotypic determinants on the autoaggressive T cells. (5) One obstacle to this approach in human disease is the polymorphism of the MHC in the species and the commensurate heterogeneity of autoimmune T cells.
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PMID:Neurological autoimmune disease and the trimolecular complex of T-lymphocytes. 266 95


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