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)

Incubation with specific antigen, myelin basic protein, greatly enhances the ability of guinea pig peritoneal exudate cells to transfer experimental allergic encephalomyelitis. Reproducibly successful transfers are obtained with 10(7) cells. With this relatively small number of cells, in vitro studies to determine the immunologic mechanisms involved in the disease process are now possible.
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PMID:Transfer of experimental allergic encephalomyelitis with guinea pig peritoneal exudate cells. 8 76

Experimental allergic encephalomyelitis (EAE) was studied in guinea pigs with an inherited deficiency of the fourth component of complement (C4) and in guinea pigs injected with cobra venom factor to deplete the third component and late-acting components of complement. EAE was elicited by immunization with homologous spinal cord or purified basic protein. Administration of cobra factor after the injection of encephalitogenic emulsion delayed the onset and reduced the intensity of the clinical manifestations of EAE. In addition, cobra factor markedly reduced mortality during the sixty days of observation. However, pathological changes of perivascular infiltration and demyelination were similar in cobra factor-treated and untreated animals. Clinical signs of EAE an mortality in C4-deficient guinea pigs were no different from those in normocomplementemic controls. Thus, although activation of the classic complement pathway does not appear to be involved in the production of EAE in guinea pigs, our results suggest a possible role of the alternative complement pathway in the pathogenesis of EAE.
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PMID:Experimental allergic encephalomyelitis in cobra venom factor-treated and C4-deficient guinea pigs. 8 12

Spleen cells from myelin basic protein (BP)-sensitized donor rats appear to be incapable of adoptively transferring experimental allergic encephalomyelitis (EAE) directly to normal recipients. It has been reported that in vitro incubation with concanavalin A (Con A) activates rat spleen cells so that they are capable of transferring EAE. We report here that incubation with specific antigen, BP, also permits transfer of disease with spleen cells. Data are presented in which activation of EAE spleen cells by Con A is compared with activation by BP. Cellular proliferation does not appear to be necessary for in vitro activation with specific antigen.
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PMID:Adoptive transfer of experimental allergic encephalomyelitis: incubation of rat spleen cells with specific antigen. 8 24

We report characteristics of the cerebrospinal fluid (CSF) pleocytosis (616+/-148 cells/microliter) that occurred in guinea-pigs with definite clinical experimental allergic encephalomyelitis developing 12 to 16 days after sensitization with homologous myelin basic protein. This pleocytosis was not present in the cerebrospinal fluid of a group of animals studied when still healthy, 9 or 10 days after similar sensitization. Eighty-nine per cent of cells in the CSF pleocytosis were small lymphocytes, 8% were larger lymphocytes and the remainder mostly monocytes. Of the lymphocytes, most were E-rosetting or null cells. B-cell markers were uncommon. The cellular patterns in this CSF pleocytosis appear to be similar to those seen in some delayed hypersensitivity responses.
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PMID:Cerebrospinal fluid lymphocytes in experimental allergic encephalomyelitis. 8 1

Groups of juvenile Strain 13 guinea pigs sensitized for chronic relapsing experimental allergic encephalomyelitis (EAE) with isogeneic central nervous system (CNS) tissue in complete Freund's adjuvant (CFA) were either left to develop late-onset chronic EAE (unsuppressed), or given a series of injections of bovine myelin basic protein (MBP) in incomplete Freund's adjuvant (IFA) to suppress the disease. All unsuppressed animals developed disease and all suppressed animals remained healthy over a 27-month period of study. some unsuppressed and suppressed animals were rechallenged with CNS tissue in CFA 12 or 26 months post-inoculation (PI). Unsuppressed animals all became sick 2-4 weeks after rechallenge, while rechallenged, suppressed animals were protected, indicating that the suppression was permanent. Pathologic findings in the CNS complemented the clinical changes. Circulating lymphocyte studies were performed on animals from all groups. Early (active, high-affinity rosetting) T cell levels in unsuppressed animals showed significant decreases during exacerbations (P less than 0.01) and normal values during remissions. After rechallenge, circulating early T cells decreased in unsuppressed animals with the development of signs. In suppressed animals, early T cells showed significant elevations during, and for a short time after, the period of suppressive injections, and normal values afterwards. These levels did not change significantly after rechallenge. Late (total, 24 hour rosetting) T cell and B cell values showed minor fluctuations only which did not correlate with disease activity. These results indicate that chronic relapsing EAE can be successfully suppressed with MBP in IFA, that this suppression is permanent and that the immunologic findings presented correlate well with the clinical and pathologic facets of the disease. the findings are presented in terms of their relevance to multiple sclerosis.
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PMID:Chronic relapsing experimental allergic encephalomyelitis. Correlation of circulating lymphocyte fluctuations with disease activity in suppressed and unsuppressed animals. 8 2

We have developed a quantitative assay for experimental allergic encephalomyelitis (EAE) in the rat based on permeability of the spinal cord to 125I-human gamma-globulin (HGG). This assay is highly reproducible and eliminates many of the drawbacks of assaying for EAE on the basis of clinical and/or histologic criteria. Using the assay, we have shown a direct correlation between onset of histologic changes in the spinal cord and onset of permeability changes in the spinal cord. No rat without histologic lesions manifest permeability alterations, and all rats with histologic lesions did manifest increased permeability to 125I-HGG. Furthermore, strains of rats susceptible to EAE demonstrated permeability changes, whereas resistant rats did not. In addition, we demonstrated by permeability and histologic criteria that guinea pig myelin basic protein emulsified with incomplete Freund's adjuvant is encephalitogenic in the Lewis rat. We also demonstrated that recipients of passive transfer of sensitized cells develop permeability changes along with histologic lesions. We conclude that measuring permeability to 125I-HGG in the spinal cords of rats is a valid assay for EAE, and its improves upon current indices of EAE in that it is readily quantifiable.
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PMID:A quantitative assay for experimental allergic encephalomyelitis in the rat based on permeability of spinal cords to 125I-human gamma-globulin. 8 21

Isolated myelin basic protein (MBP) was less effective than an equivalent amount of spinal cord in inducing protection against experimental allergic encephalomyelitis produced by a challenge of either cord, purified myelin or MBP. Complete protection was only obtained when an MBP challenge was preceded by spinal cord treatment. There was a 100% incidence of disease in the guinea pigs pretreated with MBP before challenge with spinal cord or myelin, but the onset was delayed by 3--4 weeks and the disease was less severe than in the controls. Recurrent disease was seen in some control and pretreated animals challenged with spinal cord but not in animals challenged with MBP.
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PMID:Relative effectiveness of spinal cord and purified myelin basic protein in producing resistance to experimental allergic encephalomyelitis. 8 69

We have extended earlier studies on the suppression of clinically evident experimental allergic encephalomyelitis (EAE) in monkeys, repeated injections of human basis protein. The results confirm that after suppressive treatment, recovered animals remain clinically normal and do not show spontaneous recurrence of symptoms. However, recovered animals are susceptible to EAE upon renewed challenge, and they develop the disease more rapidly and more severely than after the initial challenge; resuppression is also accomplished in these cases by the same methods used previously. The results indicate further that the basic protein or peptide T administered without mycobacteria is effective in suppressing the development of basic protein-induced EAE regardless of the species from which it was derived.
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PMID:Suppression and reversal of allergic encephalomyelitis in rhesus monkeys with basic protein and peptides. 8 79

A series of peptides, produced from peptide 68-88 by selective enzyme cleavage, were used to define the amino acid sequences required for the induction of experimental allergic encephalomyelitis (EAE), an in vitro lymphocyte proliferative response (LPR), and serum antibody by peptide 68-88 in the Lewis rat. Here we present data that indicate that the T cell determinants for induction of EAE, an LPR, and helper function in the production of antibody are located in the same region of the molecule and that a minimum of 13 amino acids are involved; i.e., residues 71-85.
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PMID:The immune response of Lewis rats to peptide 68-88 of guinea pig myelin basic protein. I. T cell determinants. 9 87

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


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