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)

Myelin basic protein (MBP) of guinea pig origin was incorporated into magnetically responsive albumin microspheres. Protein-protein bonding and stabilization of the GPMBP microspheres by heating at 120 degrees C did not adversely influence their capacity to bind anti-MBP antibodies or demonstrably alter the encephalitogenic activity of the incorporated GPMBP. The magnetic properties of the particles and the fact that immunodeterminants of some of the incorporated MBP fortuitously were distributed on the exterior surfaces of the microspheres allowed a number of experiments to be carried out in Lewis rats for the first time: (a) selective capture and deletion of that particular subpopulation of lymphoid cells responsible for transfer of experimental allergic encephalomyelitis (EAE) represented within the lymph node cells (LNC) of donor animals sensitized to neutral antigen, (b) enhancement of in vivo uptake of MBP by macrophages (M phi s) contained in oil-induced peritoneal cell exudates and exposed briefly to MBP microspheres, and (c) preparation of cell suspensions specifically enriched with respect to MBP-containing M phi s.
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PMID:Albumin magnetic microspheres: a novel carrier for myelin basic protein. 618 46

The autoimmune disease of the central nervous system (CNS), experimental allergic encephalomyelitis (EAE), is induced by challenge of genetically susceptible animals with spinal cord homogenates or myelin basic protein (MBP). Chronic and relapsing forms of the disease have some similarities to human demyelinating disorders, namely, multiple sclerosis, and are of particular interest. EAE can be transferred passively with sensitized lymphoid cells into syngeneic animals but transferred EAE has been believed to have limited relevance to human disease because it is usually monophasic and manifested by minimal demyelination. We report here that a single transfer of MBP-sensitized lymph node cells or T cell, in the absence of a peripheral antigen depot, leads to both acute EAE with significant primary demyelination, and chronic relapsing disease with lesions typical of demyelination over a long period. These findings have major implications for the immunological mechanisms involved in experimental and human demyelinating diseases.
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PMID:Adoptive transfer of myelin basic protein-sensitized T cells produces chronic relapsing demyelinating disease in mice. 620 39

The fine structure is described of a new model of chronic relapsing experimental allergic encephalomyelitis in the SJL/J mouse induced by the single adoptive transfer of myelin basic protein-sensitized lymph node cells. The neuropathology of the condition compared favorably with that seen in other species, and unlike a similar disease in the same strain of mouse induced by active sensitization with a central nervous system emulsion, there was little axonal pathology. Typical of mouse experimental allergic encephalomyelitis was the consistent involvement of polymorphonuclear leukocytes and extravasated material in central nervous system lesions. Remissions showed remyelination to be the major feature in the central nervous system, and clinical relapses were matched pathologically by fresh waves of inflammation and demyelination. Unusually large, apparently organized, sinusoidal collections of lymphoid cells (some of them displaying evidence of proliferation) were seen in the periventricular areas of the brain. The ability to induce chronic relapsing demyelination by passive means indicates that an antigen depot is not necessary for the perpetuation of the disease which is possibly transferred by memory cells in the inoculum. This model has virtue in its applicability to the pathogenesis and therapy of multiple sclerosis.
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PMID:Adoptively transferred chronic relapsing experimental autoimmune encephalomyelitis in the mouse. Neuropathologic analysis. 620 9

Lewis rats primed with myelin basic protein (MBP) in complete Freund's adjuvant develop experimental allergic encephalomyelitis (EAE) and suddenly recover 15 to 17 days later. It was previously found that nondraining lymph node (non-DLN) cells taken at the time of convalescence and transferred into syngeneic normal animals inhibit the subsequent induction of EAE. In this report, it is shown that a suppressive factor can be extracted from non-DLN cells which mimics the inhibitory effect of cells when injected into the recipients. Non-DLN cells keep their suppressive activity on the induction of EAE after a culture of 48 h but their supernatant of culture failed to exert any protective effect in vivo. However, in vitro both the culture supernatant and the suppressor cells were found to have an inhibitory effect on the proliferative response of immune lymphoid cells to the antigen (MBP).
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PMID:Suppressor cells in Lewis rats with experimental allergic encephalomyelitis: prevention of the disease and inhibition of lymphocyte proliferation by the suppressor cells or their products. 621 77

Spinal cord sections from Lewis rats with acute experimental allergic encephalomyelitis (EAE) showed greatly increased staining of astrocytes when stained immunocytochemically for glial fibrillary acidic protein (GFAP). Fibrous processes in white matter were heavily stained early in the course of the disease when paralysis was first evident (10-12 days after injection of guinea pig spinal cord myelin), then protoplasmic astrocytes were stained in the gray matter and became more heavily stained at 20 days post-injection. The stained astrocytes were evenly distributed throughout the tissue, and did not correspond to the sites of the lesions. Spinal cord slices of control and EAE rats were incubated with [3H]amino acids, then cytoskeletal proteins were prepared in an enriched fraction, separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), and the protein bands counted for radioactivity. In the EAE rat all cytoskeletal proteins, including the neurofilaments, vimentin, microtubules, GFAP and actin, showed increased uptake of radioactive amino acids. Immunoprecipitation of GFAP with specific antiserum showed increased radioactivity in the complex beginning at day 10 when cellular infiltration was beginning in the EAE animals. As the disease became acute, the radioactivity in the immunoprecipitated GFAP increased, in some cases to very high levels, then by day 18 when recovery was underway, the radioactivity had fallen to normal levels. Possible agents causing metabolic activation of protein synthesis in EAE animals include stimulating substances elaborated by infiltrating lymphoid cells, and the generalized edema accompanying the demyelinative condition. The activation of GFAP protein staining and metabolism in EAE might serve as a model for the activated growth of astrocyte processes which cause the severe gliosis seen in multiple sclerosis.
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PMID:Immunocytochemical staining for glial fibrillary acidic protein and the metabolism of cytoskeletal proteins in experimental allergic encephalomyelitis. 634 9

Vascular elements were isolated from the brain white matter of rats with acute experimental autoimmune encephalomyelitis following transfer of activated myelin basic protein-specific syngeneic T line lymphocytes. Fractions containing highly purified capillary and small postcapillary vessels and fractions enriched for perivascular infiltrates ("cuffs") were obtained using equilibrium density gradient centrifugation to remove myelin and 1 X g sedimentation in a fetal calf serum gradient to sort the vascular elements. Immunocytochemical analysis revealed that capillary cells were negative for Ia determinants. In small postcapillary vessels with scanty lymphoid cell infiltration, Ia expression was restricted to circumscript areas, often, but not always, around adhering lymphoid cells. Immunocytochemistry combined with cytofluorometry established that the majority of all perivascular lymphocytes expressed the phenotype W3/25, defining either helper T cells or T cells involved in delayed-type hypersensitivity. Less than 3% of the lymphocytes were positive for OX8, which defines suppressor and cytotoxic T subsets. Membrane immunoglobulin expressing B lymphocytes were also less than 10% of the infiltrating cells.
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PMID:The lesion of acute experimental autoimmune encephalomyelitis. Isolation and membrane phenotypes of perivascular infiltrates from encephalitic rat brain white matter. 637 91

Subpopulations of lymphoid cells were compared with respect to their ability to migrate into the central nervous system (CNS) of mice with acute experimental allergic encephalomyelitis (EAE). In mice with established lesions, the majority of cells homing to the CNS are not presensitized to CNS antigens. B cells had a much reduced capacity to migrate into the CNS of sick mice compared with T cells. However, T cells of both the Lyt-2+ and Lyt-2- subsets homed equally well to the CNS. The relative paucity of B cells in the lesions of EAE and multiple sclerosis may thus partly result from the limited ability of these cells to migrate into the CNS across the blood-brain endothelial barrier. The predominance of Lyt-2- T cells over Lyt-2+ cells in these CNS lesions is unlikely to result from such a difference in homing capacity, but may reflect the ratio of these two cell types in the blood or preferential in situ expansion of the Lyt-2- population.
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PMID:Homing of Lyt-2+ and Lyt-2- T cell subsets and B lymphocytes to the central nervous system of mice with acute experimental allergic encephalomyelitis. 660 64

Inhibitors of proteolytic enzymes were tested for their ability to suppress the clinical signs and CNS lesions produced by injection of purified myelin in complete Freund's adjuvant into Lewis rats. Pepstatin or a series of neutral protease inhibitors including aprotinin, soybean trypsin inhibitor, leupeptin, antipain, trans-aminomethyl cyclohexane carboxylic acid (AMCA), epsilon-amino caproic acid (EACA) nitrophenyl guanidino benzoate (NPGB), D- and L-polylysine, or a new commercial protease inhibitor, dipropionyl Rhein (DPR) were injected daily beginning on day 7 after immunization of rats with myelin. Aprotinin and soybean trypsin inhibitor exacerbated the symptoms and lesions of experimental allergic encephalomyelitis (EAE), leupeptin and antipain had no effect, and the plasminogen activators AMCA, EACA, NPGB, as well as poly-L- and poly-D-lysine and DPR suppressed various aspects of EAE. The measurement of acid protease as a biochemical method for quantitation of the degree of cellular infiltration into the CNS is proposed, and the results with the various treatments presented. AMCA and NPGB may exert their effects at the site of entrance of the lymphoid cells into the CNS.
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PMID:Observations on the effects of protease inhibitors on the suppression of experimental allergic encephalomyelitis. 675 Apr 29

Experiments designed to assess the importance of age of donors and recipients in cellular transfer of experimental allergic encephalomyelitis (EAE) in inbred Lewis rats indicate: (a) that lymph node cells (LNC) of suckling rats sensitized to neuroantigen-adjuvant are just as effective in transfer of the disease to adult recipients as LNC from similarly sensitized adult donors, (b) that EAE can be transferred to suckling rats just as well as adults using lymphoid cells from either suckling or adult donors, and (c) while relatively low numbers of sensitized splenocytes from suckling or adult donors may transfer EAE, relatively large numbers of spleen cells do not. Based on additional EAE transfer experiments, in which recipients received combinations of sensitized LNC and normal splenocytes, no evidence could be secured that the spleen exerts a suppressive influence on cellular transfer of the disease in Lewis s may transfer EAE, relatively large numbers of spleen cells do not. Based on additional EAE transfer experiments, in which recipients received combinations of sensitized LNC and normal splenocytes, no evidence could be secured that the spleen exerts a suppressive influence on cellular transfer of the disease in Lewis s may transfer EAE, relatively large numbers of spleen cells do not. Based on additional EAE transfer experiments, in which recipients received combinations of sensitized LNC and normal splenocytes, no evidence could be secured that the spleen exerts a suppressive influence on cellular transfer of the disease in Lewis rats.
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PMID:Cellular transfer of experimental allergic encephalomyelitis employing suckling and adult Lewis rats. 697 35

Previous claims that experimental allergic encephalomyelitis (EAE) was enhanced by essential fatty acid (EFA) deficiency were reinvestigated. Deficiency was induced in Lewis rats by feeding a fat-free diet starting in late gestation, at weaning or in adult life with or without a previous period of starvation. Retardation of growth, the typical dermatitis, increased water consumption and testicular atrophy gave evidence of EFA deficiency. Control rats were fed a complete diet or a fat-free diet supplemented with corn oil. EAE was induced in EFA-deficient and control rats by conventional active sensitization with neural antigen and adjuvants or by passive transfer of living lymphoid cells from sensitized nutritionally normal donors. Contrary to previous reports, EFA deficiency did not enhance EAE in any of seven experiments, and these results were supported by histological examinations. In fact, we found inhibition of clinical signs, but not histological lesions, when EFA deficiency was moderately advanced. This was accompanied by (and probably related to) thymic atrophy, possibly due to nonspecific stress. Also we found that EFA deficiency had no effect on a non-immunological model of brain inflammation that resembles EAE in the occurrence of lymphocytic infiltrates.
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PMID:Effect of essential fatty acid deficiency on experimental allergic encephalomyelitis in rats. 737 35


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