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

Complement-dependent demyelinating activity of whole brain homogenate (WBH)-induced experimental allergic encephalomyelitis (EAE) sera was tested on long term tissue cultures of in vitro myelinated fetal guinea pig cerebellum. Complement-fixing (CF) auto-antibodies were shown to be the responsible agents, as demonstrated in experiments where all reagents belonged to the same species: guinea pigs of outbred (Hartley) and even of inbred (S2 or S13) strains. These antibodies were of the IgG2 class as shown by Sephadex G-200 and DEAE cellulose fractionation experiments. The corresponding auto-antigen was present in the homogenate and myelin of the central nervous system (CNS) tissue. It was different from the encephalitogenic basic protein of CNS myelin (BP), as shown in experiments where the demyelinating auto-antibodies were induced, detected, and absorbed by WBH or by CNS myelin but not by BP. They were neither induced by nor cross-reacting with cerebroside and peripheral nervous system (PNS) tissue.
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PMID:Studies on autoimmune encephalomyelitis in the guinea pig. II. An in vitro investigation on the nature, properties, and specificity of the serum-demyelinating factor. 5 35

Previous studies have shown that peritoneal inflammatory exudate cells from guinea pigs with experimental allergic encephalomyelitis proliferate prominently when cultured with the sensitizing myelin basic protein. Peripheral blood lymphocytes (PBL) obtained at the same time responded little, if at all. In the present studies, recombination experiments using appropriate mixtures of peritoneal exudate macrophages and PBL show that the presence of such macrophages will not enhance in vitro reactivity of the PBL to basic protein. The oil-induced peritoneal inflammatory response appears to deplete the PBL somewhat of antigen-reactive lymphocytes, but does not totally explain the difference in in vitro responsiveness between the lymphocytes in the peritoneal exudate and in the peripheral blood.
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PMID:Reactive and nonreactive lymphocytes in experimental allergic encephalomyelitis. I. Possible role of macrophage-lymphocyte interactions. 5 39

Experimental allergic encephalomyelitis (EAE) is a cell-mediated autoimmune response directed toward a component of central nervous system (CNS) tissue, myelin basic protein (BP). Injection of animals with either whole CNS tissue or purified BP in complete Freund's adjuvant (CFA) induces severe and usually fatal disease. Preimmunization of animals with BP in incomplete Freund's adjuvant (IFA) prevents EAE. We have examined the relative abilities of whole guinea pig BP and its fragments to protect guinea pigs from subsequent EAE induction. The data suggest that the presence of the intact encephalitogenic site (residues 113-121) in the molecules used for preimmunization is necessary but may not be sufficient for complete protection against EAE induction.
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PMID:Protection against experimental allergic encephalomyelitis with peptides derived from myelin basic protein: presence of intact encephalitogenic site is essential. 5 30

The induction of immunological tolerance with, and for, the caused organotypical antigen is a conception for a specific therapy for neuroimmunological diseases with at least a partial autoallergic pathogenesis. Appropriate to a set step-by-step programme for the development of antigen-specific therapy preventive tolerance experiments were carried out at the model of experimental allergic encephalomyelitis (EAEM) with allogenic myelin basic protein (BP) prepared from rabbits. The result is: 100 ug BP given intravenously simultaneously with 100 ug BP in incomplete Freud's adjuvant given intracutanously twice a week and 40 mg Cyclophosphamid given daily during the minor clinical incidence rate and no signs of EAEM pathomorphologically. A longlasting tolerance for the BP could be obtained as a test proved after 100 days. Hints are given for further potential therapeutic treatments, such as the use of antigen bound chemically to the immunosuppressive drug or the use of chemically modified BP for the induction of a specific tolerance.
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PMID:[Experimental allergic encephalomyelitis as a model for the study of therapeutic concepts for encephalomyelitis disseminata]. 5 33

Although both the T and B cells of the Lewis rat have immunoglobulin receptors for basic protein (BP) of myelin, and both cell types are required for antibody production to BP, the present results demonstrate that the T cells are the only cells required for the induction of experimental allergic encephalomyelitis (EAE). Both EAE and anti-BP were readily induced in thymectomized, irradiated Lewis rats reconstituted with normal thymus and bone marrow cells and challenged with BP in complete Freund's adjuvant. If the thymus cells were first treated with BP heavily labeled with 125I so as to eliminate (sucide) specific T cells, the recipients neither develop EAE nor produce antibody to BP. On the other hand, if the thymus cells were untreated and the specific B cells of bone marrow were eliminated by treatment with 125I-BP, EAE was not inhibited, although no antibody was produced. These results strongly suggest that the T cell is responsible for the induction of EAE although both the T and B cells are competent to respond to BP. Evidence was presented which suggests that neither suppressor T cells nor circulating antibody are involved in the inhibition of EAE by injection of Lewis rats with nonencephalitogenic preparations of BP. The immune status of T and B cells of the Lewis rat to BP was compared with the immune status of these cells in other species to thyroglobulin, where only the B cells appear to be competent. In this context, Brown Norway rats, which are resistant to the induction of EAE, also appear to lack T cells reactive to BP, although competent B cells are present.
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PMID:Cellular events in the induction of experimental allergic encephalomyelitis in rats. 6 Apr 61

A detailed description and stepwise evaluation of a procedure that can be used to obtain myelin basic protein (BP) from whole brain is presented. The procedure involved the 0.001 MHC1 extraction of whole brain pre-treated in a sequential manner with chloroform-methanol (2:1 v/v), acetone, and deionized water. This is followed by a precipitation of the extract at pH 9.0, and gel filtration of the supernatant in 0.01 M HC1. Yields of canine and porcine BP and their disc gel evaluations are presented at several key points in the procedure. The final products possessed a high degree of homogeneity when examined on SDS gels stained with commonly used protein stains. When compared with six SDS-gel marker-protein standards, the canine and porcine final products had mobilities that correspond to an apparent molecular weight of 18,5000 +/- 5%. Quantitative binding of 125I-labeled canine and porcine BPs with standardized rabbit anti-BP antisera gave comparable results. Immunoelectrophoretic and immunodiffusion examinations demonstrated single components and complete identity. The canine and porcine BP's also reacted fully with syngeneic anti-BP antisera raised in Lewis-strain rats. The canine BP was tested for encephalitogenicity in Lewis-strain rats and found to be comparable to rat BP in producing experimental allergic encephalomyelitis.
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PMID:An evaluation of a procedure for the isolation of myelin basic protein (BP). 6 Jul 58

Rats of certain strains immunized with bovine encephalitogenic protein (EP) in Freund's complete adjuvant develop an impairment of the mixed leukocyte reaction (MLR) similar to that seen in rabbits with experimental autoimmune encephalomyelitis and in humans with certain diseases, including multiple sclerosis. The rats mount a cell-bound response to EP, but encephalomyelitis does not develop. The component causing the impairment was analysed in a culture system using inbred rat strains and F1 hybrids, thoracic duct cells as a source of lymphocytes, and blood as a supplement to the cultures. In normal rats, it was shown that the effects of responding and of stimulating lymphocytes could be separated and that the supportive action of the added blood was probably due to macrophages (monocytes); also that the added blood could in many experiments be replaced with 2-mercaptoethanol (2-ME). The impairment present in immunized rats is at least largely due to a defective supportive activity of the blood (monocytes) and can be restored with 2-ME. The results argue that the MLR impairment seen in immunized rats is due to a faulty macrophage function.
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PMID:Mixed leukocyte reaction in rats. Effect of immunization with bovine encephalitogenic protein and Freund's complete adjuvant. 6 Aug 45

An attempt was made to correlate the percentages of macrophages, lymphocytes and granulocytes in the peritoneal effusion in healthy guinea pigs and guinea pigs with experimental allergic encephalomyelitis (EAE), with the macrophage migration inhibition (MMI) test. Varying percentages of the cells had no influence on values of MMI. Similarly, in guinea pigs with EAE, percentages of formed elements in peritoneal effusion were not correlated with intensity of MMI or with histopathologic lesions in the brain and spinal cord. It is suggested that the observed differences are due to individual immunologic responsiveness of animals and, probably, to other hitherto unknown mechanisms.
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PMID:Formed blood elements in peritoneal effusion and the macrophage migration inhibition test in healthy guinea pigs and in guinea pigs with experimental allergic encephalomyelitis. 6 Sep 84

Experimental allergic encephalomyelitis has been induced in guinea pigs employing bovine myelin basic protein as the antigen and a hydrosoluble tetrasaccharide-heptapeptide from delipidated cells of the human mycobacterial strain H37Ra as adjuvant. The maximum response was observed using 33 mug of antigen and 12.5 mug of adjuvant per animal.
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PMID:Induction of allergic encephalomyelitis using hydrosoluble mycobacterial fractions. 6 73

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


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