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)

New precepts gained from the crescendo of neuroimmunobiologic research of recent decades have increased our understanding of experimental allergic encephalomyelitis (EAE), virus-associated acute disseminated encephalomyelitis (ADE), and multiple sclerosis (MS). EAE of animals and humans provides evidence of the existence in mammalian lymphoid tissues of potential clones of cells with autoreactivity for myelin basic protein (MBP) and other antigenic constituents of the central nervous system (CNS). In a new hamster model, EAE has been strikingly potentiated by persistent infection of the CNS with defective measles virus, a finding that also has implications for virus-associated ADE. Endogenous MBP or MBP degradation fragments, reactive with MBP antibodies of various affinities, have been detected by a recently devised radioimmunoassay in serum, plasma, and other body fluids of normal rats, rats with EAE, and patients with virus-associated ADE or MS. Circulating MBP or MBP fragments may be of great importance in inhibiting neuroautoimmune reactivity and play a role in repair of immunologic CNS injury should it inadvertently occur. Finally, the impressive degree of concordance of immunologic events in EAE, virus-associated ADE, and MS provides additional support for the central importance of host neuroimmunologic responses in the pathogenesis of these neutologic diseases.
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PMID:Joseph E. Smadel Memorial Lecture: neuroimmunologic diseases of animals and humans. 9 35

Isolation of a viral agent (107) directly from brain explants of a 15-month-old heifer with symptoms of a sporadic encephalomyelitis is described. The virus shares properties with the paramyxovirus family. It grows in a variety of cell cultures from different species, and induces nuclear and cytoplasmic inclusion bodies in infected cells. Nucleocapsids measuring 17 nm in diameter were found in the nucleus and cytoplasm of these cells when studied electron microscopically, thus indicating a close relationship of the agent to the measles-distemper-rinderpest group. No infectious virus was released from infected cells, although alignment of nucleocapsids was observed beneath the cell membrane, and no hemagglutinating activity could be detected with the methods employed. The 107 agent was compared serologically with parainfluenza viruses type 1, 2 and 3, simian virus 5, mumps and Newcastle disease virus (NDV), two bovine respiratory syncytial viruses and measles/subacute sclerosing panencephalitis, distemper and rinderpest viruses, always using 107 virus infected CV1 cells and antiserum of the different viruses in indirect FA tests. Positive FA reactions were observed only with two sera obtained from SSPE patients with high antibody titer to SSPE virus, and with one rabbit-anti-rinderpest serum. The titers of these sera to 107 virus, however, were significantly lower than those against homologous viruses. Five out of 9 sera from randomly selected healthy cattle showed antibody titers between 1:10 and 1:80 to 107 virus in FA tests. The significance of these results is discussed with respect to the epidemiology of SSPE in children and its possible implication with rinderpest in Europe.
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PMID:Sporadic bovine meningo-encephalitis-isolation of a paramyxovirus. 16 89

To clarify mechanisms underlying acute disseminated encephalomyelitis (ADE) in patients with infection due to measles or other viruses, a new animal model was devised. Adult hamsters that had clinically recovered from acute encephalitis induced by prior intracerebral injection of the HBS strain of measles virus were challenged with neuroantigen plus adjuvant. Such hamsters, which had a high likelihood of carrying persistent HBS measles virus in the central nervous system (CNS), exhibited a significantly higher incidence of experimental allergic encephalomyelitis (EAE) following challenge as compared with simultaneously challenged but previously uninfected littermates. Occurrence of EAE in hamsters previously injected with heat-inactivated virus was not potentiated, a finding suggesting that persistence of the virus in the CNS renders that organ system more vulnerable to immunologic attack. This new model has promise for the probing of relationships between persistent viral infections of the CNS and host autoimmune responses directed against that target organ system.
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PMID:Potentiation of experimental allergic encephalomyelitis in hamsters with persistent encephalitis due to measles virus. 44 85

Beta 2-microglobulin (beta 2m) is a small protein that forms the light chain of the class I major histocompatibility molecule and is also present in soluble form in serum and cerebrospinal fluid (CSF). Measles is associated with immune activation and evidence of immunologic abnormalities that persist for several weeks. To assess further the immunologic changes occurring during measles, beta 2m was measured in plasma and CSF. beta 2m became elevated during measles before the onset of the rash and was highest during the rash. Elevations persisted for several weeks and correlated well with levels of soluble interleukin-2 receptor and neopterin and less well with soluble CD8. CSF beta 2m was elevated in postmeasles encephalomyelitis. Plasma levels of beta 2m did not correlate with spontaneous proliferation of peripheral blood mononuclear cells (PBMC) or with in vitro production of beta 2m by cultured PBMC. The data suggest that increases in beta 2m in measles correlate better with cytokine production than with cell proliferation.
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PMID:Immune activation during measles: beta 2-microglobulin in plasma and cerebrospinal fluid in complicated and uncomplicated disease. 140 29

Theiler's murine encephalomyelitis virus (TMEV) is a picornavirus which induces a chronic demyelinating disease of the central nervous system (CNS) in certain susceptible mouse strains. Demyelination has been shown to result from immunopathological responses mediated by CD4+, major histocompatibility complex (MHC) class II-restricted T cells. As little or no class II is expressed in the normal mouse CNS, the ability of astrocytes to express these proteins and present antigen to T cells from TMEV-infected mice was investigated here. It is shown that astrocytes are capable of presenting TMEV to virus-specific T cells in vitro, and that this ability is dependent on prior induction of MHC class II by interferon-gamma (IFN-gamma) treatment. Unlike other viruses such as murine hepatitis virus-JHM (a coronavirus) and measles, TMEV is not capable of inducing class II on astrocytes directly. There is a correlation between the ease of class II induction on astrocytes from different mouse strains by IFN-gamma and mouse strain susceptibility to TMEV-induced demyelinating disease. These results suggest that following viral infection and initial T-cell infiltration into the CNS, class II induction on astrocytes is a key step allowing local antigen presentation and amplification of immunopathological responses within the CNS and hence the development of demyelinating disease.
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PMID:Susceptibility to Theiler's virus-induced demyelinating disease correlates with astrocyte class II induction and antigen presentation. 162 91

Subacute encephalomyelitis (SAME) in Lewis rats following infection with a neurotropic measles virus (MV) is associated with a cell-mediated autoimmune response (CMAI) to myelin basic protein (MBP). MBP-selected CD4+ T cell lines both from measles-infected animals as well as from rats challenged with guinea pig MBP (Gp-MBP) had a similar pattern of response in the presence of synthetic peptides to Gp-MBP and specifically responded in vitro only to the encephalitogenic and not the non-encephalitogenic or other control peptides. In primary splenic lymphocyte cultures from SAME animals, however, a low but significant T-cell response was obtained against the non-encephalitogenic peptide S67 (residues 69-81) of the Gp-MBP. Moreover, immunization of MV-infected rats with this peptide induced clinical and histological experimental allergic encephalomyelitis (EAE) in 38% of the animals. The results of the study show that the non-encephalitogenic peptide S67 can be rendered encephalitogenic in rats when an additional stimulus is given in the form of MV infection. The data indicate further that MV infection of the central nervous system (CNS) enhances the susceptibility of the CNS to autoimmune T cell aggression.
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PMID:Characterization of measles virus-induced cellular autoimmune reactions against myelin basic protein in Lewis rats. 169 12

The pathogenesis of multiple sclerosis (MS) is considered from three different viewpoints: genetic, viral and immunological. A genetic predisposition intervenes, as testified by the familial forms of MS and by the frequency of HLA A3B7 and DR2 groups in MS patients. The hypothesis of an inherited enzyme deficiency in oligodendrocytes is discussed. Many viruses are known to induce demyelination in animals, and the intrathecal production of antibodies to measles virus as well as the in vitro discovery of DNA transcripts of this virus in patients are suggestive of a viral factor. Experimental allergic encephalomyelitis (EAE) and chronic EAE have made it possible to study the immune and other mechanisms which might be involved in MS. While the myelin basic protein and the M2 antigen appear to be the first antigen targets, the demyelinating agents in this model are antibodies to galactocerebroside. The factors responsible for demyelination in MS have not yet been elucidated, but the antibodies present in the cerebrospinal fluid do not seem to be demyelinating in vitro. Descriptions of the cells which constitute the lesions and of the antigen markers they express suggest that endothelial cells and astrocytes (possibly presenting antigens to lymphocytes) might play a part in the genesis of the lesions. Experiments concerning the modulation and suppression of EAE allow new therapeutic approaches to be envisaged.
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PMID:[Multiple sclerosis: review of main experimental data and pathogenic hypotheses]. 209 17

To study T cell and macrophage activity during measles, levels of interferon-gamma (IFN-gamma) and neopterin in plasma and cerebrospinal fluid (CSF) were measured. Plasma levels of IFN-gamma were elevated in measles (1.17 +/- 0.27) compared with healthy adults (0.13 +/- 0.06, P less than .05) and children (0.14 +/- 0.06, P less than .01). Plasma levels of neopterin were elevated in measles (32.5 +/- 2.7) compared with healthy adults (5.3 +/- 2.9, P less than .0001), healthy children (12.1 +/- 4.0, P less than .001), and children with other infectious diseases (20.6 +/- 4.0, P less than .02). IFN-gamma was increased in measles primarily during rash; neopterin remained elevated for several weeks. Levels of neopterin showed a significant positive correlation with plasma levels of soluble interleukin-2 receptor and soluble CD8, two other parameters of T cell activation. Children with measles complicated by pneumonia had higher levels of neopterin in serum than those with uncomplicated disease. Children with measles complicated by autoimmune encephalomyelitis had higher levels of neopterin in CSF than those with noninflammatory neurologic disease but lower than those with central nervous system infections. Thus, IFN-gamma seems to be produced in vivo during acute measles virus infection; deficiency of this lymphokine does not appear to correlate with increased susceptibility to secondary infections.
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PMID:Immune activation during measles: interferon-gamma and neopterin in plasma and cerebrospinal fluid in complicated and uncomplicated disease. 210 64

Post-infectious or post-vaccinal demyelinating encephalomyelitis and neuritis may be due to immunological cross-reactions evoked by specific viral antigenic determinants (epitopes) that are homologous to regions in the target myelins of the central and peripheral nervous systems. Such homologies have been found by computer searches in which decapeptides in two human myelin proteins were compared with proteins of viruses known to infect humans. These viruses include measles, Epstein-Barr, influenza A and B, and others that cause upper respiratory infections. Several regions identified in myelin basic protein and P2 protein can be related to experimental allergic encephalomyelitis or neuritis in laboratory animals.
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PMID:Sequence homology between certain viral proteins and proteins related to encephalomyelitis and neuritis. 240 2

The loss of myelin-associated glycoprotein (MAG) and myelin basic protein (MBP) was compared by quantitative immunocytochemistry in demyelinating lesions of measles encephalomyelitis (ME), multiple sclerosis (MS), and progressive multifocal leukoencephalopathy (PML). Serial sections from paraffin-embedded tissue were reacted with antisera for MAG and MBP, and areas of staining loss were compared morphometrically. Lesions in ME showed MAG loss equal to that of MBP, lesions of PML showed MAG loss greater than that of MBP, and MS lesions showed a mixture of patterns. These data demonstrate distinctive patterns of MAG and MBP loss in these three diseases.
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PMID:A quantitation of myelin-associated glycoprotein and myelin basic protein loss in different demyelinating diseases. 241 98


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