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)

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

The 48-hour passive cutaneous anaphylaxis (PCA) and passive anaphylactic bronchoconstriction in rats induced by an IgE-like antibody against DNP-Ascaris were inhibited by intravenous treatment with traxanox sodium in a dose dependent manner. In both experiments, traxanox sodium was more potent than disodium cromoglycate (DSCG), especially as an inhibitor of bronchial anaphylaxis. In the PCA test of rats using a double sensitization technique according to the Orr's method, traxanox sodium was demonstrated not to inhibit antigen-antibody combination, but to inhibit the release of chemical mediators at a stage following antigen-antibody combination. Traxanox sodium inhibited the complement dependent immune hemolysis, but not the hypotonic hemolysis in vitro. However it failed to inhibit the Forssman anaphylaxis in the guinea pig in vivo. Traxanox sodium (50-250 mg/kg p.o.) showed an inhibitory effect on the direct passive Arthus reaction (DPAR) of the rats. Furthermore, it delayed the onset of the hyperacute form of experimental allergic encephalomyelitis (EAE) and reduced mortality in the rats. DSCG was less effective on DPAR and EAE. In conclusion, traxanox sodium is considered to have a wider spectrum of anti-allergic activity than DSCG since it has a suppressive effect not only on the type I allergic reaction, but also on the type III and IV allergic reactions.
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PMID:[[Effect of traxanox sodium on type I-IV allergic reactions. Studies on anti-allergic agents VII]. 621 52

Rabbit antisera against normal guinea pig lymph node, when injected into guinea pigs, produced transient depression of the level of blood lymphocytes. It had no effect on other circulating cellular elements. Repeated injection over several days produced lymphopenia, which became progressively less marked with continued treatment, and clear-cut depletion of small lymphocytes in lymph nodes, whether draining an inoculation site or remote. In guinea pigs treated with lymphocyte antiserum, there was marked suppression of the tuberculin and contact allergic reactions and the "delayed" skin reaction to purified diphtheria toxoid, and a relative suppression of allergic encephalomyelitis and the rejection of first set skin homografts. There was a slight effect on second set graft rejection and no effect on PCA or the reversed passive Arthus reaction. Non-specific reactions to intradermal turpentine or to concentrated dinitrochlorobenzene placed on the skin were moderately reduced. The suppression of these reactions (except allergic encephalomyelitis) was closely correlated with the degree of lymphopenia. Lymphocyte antiserum absorbed with normal blood white cells lost both its lymphopenic effect and its ability to suppress the tuberculin reaction. It is tentatively concluded that a circulating mononuclear cell, probably the small lymphocyte, is the primary reactant in the various types of delayed hypersensitive reactions.
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PMID:The use of specific "lymphocyte" antisera to inhibit hypersensitive reactions of the "delayed" type. 1400 86

Erythro-sphingosine was obtained from sphingomyelin by alkaline hydrolysis. N-p-nitrobenzoyl-sphingosine, N-p-aminobenzoyl-dihydrosphingosine and dihydrosphingosine-protein were synthesized.It was found that dihydrosphingosine-protein can produce a specific antibody which can be detected by the complement fixation test and by Ouchterlony's double diffusion method in agar. The determining factor of dihydrosphingosine may be due to the hydroxy groups at C(1) and C(3).In the course of experimental allergic encephalomyelitis, the cross-reactivity of rabbit antisera against spinal cord, and with psychosine-protein in particular, was observed by the complement fixation test and by the Arthus reaction.
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PMID:Antigenic properties of a synthetic protein complex with glycolipids and related substances. 1780 83

The complement system is important for the host defence against infection as well as for the development of inflammatory diseases. Here we show that C1q/TNF-related protein 6 (CTRP6; gene symbol C1qtnf6) expression is elevated in mouse rheumatoid arthritis (RA) models. C1qtnf6(-/-) mice are highly susceptible to induced arthritis due to enhanced complement activation, whereas C1qtnf6-transgenic mice are refractory. The Arthus reaction and the development of experimental autoimmune encephalomyelitis are also enhanced in C1qtnf6(-/-) mice and C1qtnf6(-/-) embryos are semi-lethal. We find that CTRP6 specifically suppresses the alternative pathway of the complement system by competing with factor B for C3(H2O) binding. Furthermore, treatment of arthritis-induced mice with intra-articular injection of recombinant human CTRP6 cures the arthritis. CTRP6 is expressed in human synoviocytes, and CTRP6 levels are increased in RA patients. These results indicate that CTRP6 is an endogenous complement regulator and could be used for the treatment of complement-mediated diseases.
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PMID:CTRP6 is an endogenous complement regulator that can effectively treat induced arthritis. 2640 64