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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rabbits were sensitized or immunized with a variety of central nervous system antigens, including bovine spinal cord, bovine, monkey, human, guinea pig, rabbit and rat S myelin basic proteins, and a polypeptide derived from guinea pig basic protein. The animals were observed for development of experimental allergic encephalomyelitis, and their sera were collected at varying intervals after inoculation and evaluated for presence of precipitating anti-basic protein antibody and for their ability to inhibit myelin formation in cerebellar tissue cultures. The resulting complete dissociation between development of experimental allergic encephalomyelitis, the presence of anti-basic protein antibody and the occurrence of myelination inhibition factor suggests that myelination inhibition factor is not involved in the pathogenesis of experimental allergic encephalomyelitis, and argues against a role for anti-basic protein antibody as an antimyelin factor in vitro.
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PMID:Neural antigens and induction of myelination inhibition factor. 4 59

The immunopathogenesis of experimental allergic encephalomyelitis (EAE) is reviewed with special focus on the role of central nervous system fibrin deposition in the inflammatory cascade characterizing this autoimmune disease. Among rats sensitized to whole spinal cord or myelin basic protein of either guinea pig or bovine origin, there is a striking degree of concordance of perivascular fibrin deposits and occurrence of clinical paralytic signs. Neither paralytic signs nor fibrin deposition are temporally related to development of perivascular cellular infiltrates. Rats sensitized to neuroantigen and treated with ancrod, a polypeptide derived from the venom of Agkistrodon rhodostoma, develop profound hypofibrinogenemia, have a marked inhibition of fibrin deposition, and often exhibit no paralytic signs whatsoever. In contrast, cellular infiltrates are not demonstrably influenced by ancrod treatment. Activation of the clotting cascade at loci of developing immune injury of nervous tissue appears to result from and lead to increasing neurovascular permeability and accumulation of edema fluid. Distention of the extracellular space in central and peripheral nervous system tissues by edema fluid appears to be directly responsible for clinical abnormalities characterizing EAE in rats. Cellular infiltrates, on the other hand, appear to be an independent immune response to neuroantigenic sensitization.
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PMID:Experimental allergic encephalomyelitis: role of fibrin deposition in immunopathogenesis of inflammation in rats. 6 95

Experimental autoimmunity of the CNS has been well characterized--the antigen has been identified, effector cell specificity has been defined, and the relationship between cellular sensitization and antibody production has been partially clarified. In the guinea pig, experimental allergic encephalomyelitis (EAE) is induced by one injection of myelin basic protein in complete Freund's adjuvant (BP/CFA). If BP/CFA is preceded by repeated injections of basic protein in incomplete Freund's adjuvant (BP/IFA), EAE is not induced; the guinea pigs survive and ultimately produce antibody. Induction and prevention of EAE as well as antibody induction by this schedule are dependent on the presence of the intact encephalitogenic (T-cell) site in the polypeptide used for sensitization and preimmunization. In contrast, B cell sites (those peptide sequences which bind antibody) are independent of the T-cell site. At least 5 specific antigenic regions (B-cell sites) have been demonstrated in the BP molecule. High mycobacteria levels bypass the specificity requirement of helper T-cells but cannot bypass the specificity requirement of effector T-cells. In spite of the sophisticated immunologic techniques available, our knowledge of humoral and cellular sensitivity in multiple sclerosis (MS) patients is very limited. The experimental demonstration of an analogy between EAE and MS is weak: a) Demonstration of BP-sensitized cells or BP-specific antibodies in peripheral blood of MS patients has not been successful. b) Anti-myelin serum factors reported to be associated with both disease states (experimental autoimmunity and MS) are clearly not identical. Nevertheless, successful treatment of EAE in animals by BP/IFA injections has encouraged consideration of clinical trials to test the therapeutic value of BP injections in MS patients. If successful, the question will be answered: if unsuccessful, the dilemma still remains.
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PMID:Autoimmunity in multiple slcerosis: do we have an experimental model? 8 Sep 41

Cop 1, a synthetic polypeptide, was evaluated for its effect on a chronic relapsing form of experimental allergic encephalomyelitis (EAE). Pretreatment of juvenile Strain 13 guinea pigs with Cop 1 in incomplete Freund's adjuvant (IFA) which were subsequently challenged with guinea pig spinal cord in complete Freund's adjuvant (CFA) had a marked effect in delaying or preventing the appearance of clinical signs of EAE. Administration of Cop 1 on appearance of clinical signs of EAE prevented progression of the first episode of the disease. Although relapses were not always prevented, they were modified on their duration and intensity both clinically and histologically.
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PMID:The effect of Cop 1, a synthetic polypeptide, on chronic relapsing experimental allergic encephalomyelitis in guinea pigs. 9 Jan 29

The effect of sulphydryl reagents on haemagglutinating encephalomyelitis virus (HEV), a coronavirus of pigs, was investigated. Using increasing concentrations of dithiothreitol (DTT), 50% of the virus infectivity and haemagglutination (HA) activity could be removed by i.5 mM and 4 to 5 mM respectively. The effect of DTT concentrations on the polypeptide composition was also examined. Of the three external glycoproteins gp 125 was found to be the most susceptible, 50% being removed by incubation of the virus with 5 to 6 mM-DTT. Of the other two glycoproteins gp 180 was unaffected by DDT concentrations up to 100 mM and the amount of gp 100 gradually declined at concentrations above 20 mM. The rates of removal of the virus HA activity and gp 125 suggested that this polypeptide was an essential part of the virus haemagglutinin. The lack of evidence for any interpeptide disulphide bonds suggested that the loss of these glycoproteins was due to an alteration in their conformation brought about by the cleavage of intrapeptide disulphide bonds. The loss of protein from the surface of the virus resulted in a change in the virus morphology with the appearance of thin fibrous projections instead of the characteristic petal-like coronavirus projections.
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PMID:Effect of sulphydryl reagents on the biological activities, polypeptide composition and morphology of haemagglutinating encephalomyelitis virus. 56 74

Rabbit sera against antigens prepared from the brain and the spinal cord antigens were investigated in a cytotoxic test with mouse and guinea pig lymphocytes. None of the sera exerted a cytotoxic effect on the bone marrow lymphocytes. The sera against mouse brain and spinal cord and guinea pig brain and myelin isolated from it exerted the greatest cytotoxic activity; the cytotoxicity was maximum against the thymocytes, less pronounced against the lymph node lymphocytes, and least--against the spleen cells. The cytotoxicity of the sera against the bovine spinal cord homogenate, myelin and the basic protein isolated from it was the minimal and equal with lymphocytes from any of the three mentioned sources. The serum against the encephalitogenic polypeptide 2c was practically devoid of the cytotoxic activity. The encephalitogenic activity of the 2c fraction was greater than that of the myelin and basic protein from the bovine spinal cord. Experiment of antibrain serum absorption suggested that the brain cortex contained a cross-reacting antigen. The subcutaneous injection of a relatively high dose (224 x 10(6)) of thymocytes in the complete Freund's adjuvant failed to induce the development of allergic encephalomyelitis in guinea pigs.
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PMID:[Cytotoxicity of sera against brain and spinal cord antigens in relation to lymphocytes of varying origin]. 102

A basic protein has been purified from the CNS myelin of the gummy shark (Mustelus antarticus). Electroblotting was used to examine the capacity of rabbit antisera raised against this electrophoretically pure protein to recognize myelin basic protein from higher vertebrates. The antisera bound to two shark proteins including the original polypeptide antigen and to chicken, bovine, and human myelin basic proteins. Thus, the shark protein appeared to possess antigenic determinants that have been retained through evolutionary divergence of these proteins. Whereas bovine basic protein caused experimental allergic encephalomyelitis in guinea pigs, animals that received injections of the shark protein showed neither clinical nor histological signs of this disease. However, tests for delayed-type hypersensitivity and for Arthus reaction following injection with the shark protein revealed a T-cell-mediated response to this antigen and substantial cross-reactivity with higher vertebrate basic proteins. Analysis of the amino acid composition of the shark protein, and comparison of its tryptic peptide map with that of the bovine protein, revealed substantial changes in the amino acid sequence. Although the shark protein has some antigenic determinants in common with the proteins from higher vertebrates, it appears that much of the structure differs.
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PMID:Evolutionary divergence in the structure of myelin basic protein: comparison of chondrichthye basic proteins with those from higher vertebrates. 241 3

Encephalitogenic, immunogenic properties of the polypeptide fraction of myelin basic protein (FBP) and CNS lesions have been examined in animals with experimental allergic encephalomyelitis (EAE). FBP was isolated from bovine spinal cord using column chromatography. Administration of 1.0 or 0.1 microgram FBP mixed with complete Freund adjuvant caused neurological and histological EAE manifestations in 76% and 26% of guinea-pigs, respectively. Circulating anti-FBP antibodies were not found in sensitized animals, whereas the incidence and intensity of skin reaction of delayed type hypersensitivity to FBP correlated with the development of EAE and the onset of the disease. Perivascular cell infiltration and demyelination noted in the spinal cord and brain of guinea-pigs were similar to those observed after inoculation of the brain white matter or brain tissue homogenate.
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PMID:[Immunomorphological characteristics of experimental allergic encephalomyelitis induced by an encephalitogenic polypeptide]. 243 38

COP-1 is one of a series of polypeptide preparations developed to stimulate myelin basic protein (MBP), a natural component of the myelin sheath. MBP in Freund's complete adjuvant induces experimental allergic encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). In saline, MBP suppresses EAE. This is the rationale for the use of COP-1 in MS.
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PMID:Clinical experience with COP-1 in multiple sclerosis. 329 Jul 17

The V-1 strain of Vilyuisk virus, isolated from the cerebrospinal fluid of a chronic case of encephalomyelitis in Siberia and subsequently passaged 41 times in mice, was examined to determine its serological relationship to Theiler's murine encephalomyelitis virus (TMEV) and encephalomyocarditis (EMC) virus and some physicochemical characteristics of the virion. On the basis of virion size (28 nm), icosahedral symmetry, buoyant density (1.33 g/ml), sedimentation coefficient (150S), and capsid polypeptide profile, Vilyuisk virus appears to belong to the family Picornaviridae. Acute phase mouse antisera were used to study the antigenic relatedness of Vilyuisk, GDVII (the prototypic strain TMEV), and EMC viruses by enzyme-linked immunosorbent assay (ELISA). The results indicate that Vilyuisk and GDVII viruses are similar but distant subtypes, and that Vilyuisk and EMC viruses are unrelated.
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PMID:Characterization of Vilyuisk virus as a picornavirus. 619 11


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