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)

Defined peptide fragments were isolated from the N-terminal half of the myelin basic protein (BP) molecule and employed for antigen-induced inhibition of experimental allergic encephalomyelitis (EAE). Guinea pigs pretreated with peptide 44-89, obtained by limited pepsin digestion and purified by column chromatography, were significantly protected against EAE subsequently induced by sensitization with BP in complete Fruend's adjuvant. Peptide 1-20, derived by cyanogen bromide cleavage, did not inhibit EAE, nor did the synthetic EAE peptide (residues 114-122), although this peptide was only weakly encephalitogenic for guinea pigs. These findings directly support our previous conclusion that different sites on the BP molecule are responsible for induction and inhibition of EAE, and suggest that disease inhibition can be attributed, at least in part, to a site within peptide 44-89.
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PMID:Antigen-induced inhibition of experimental allergic encephalomyelitis. III. Localization of an inhibitory site distinct from the major encephalitogenic determinant of myelin basic protein. 4 41

Myelin basic proteins and peptides derived from them by limited cleavage with pepsin were tested for their ability to induce experimental allergic encephalomyelitis (EAE) in Lewis rats. The encephalitogenicity of the weakly active bovine protein was found to be associated with both halves of the molecule, peptides (1-88) and (89-169). Of the four smaller derivates of peptide (1-88), peptides (1-36), (43-88), (1-42), and (37-88), only the last two were active. This demonstrated that the overlap region consisting of residues 37-42 (sequence Asp-Ser-Leu-Gly-Arg-Phe) constitutes an encephalitogenic determinant. Of the two smaller derivatives of peptide (89-169), peptides (111-169) and (89-152), only the last was active. This indicated that the second encephalitogenic determinant begins between residues 88 and 111 and ends before residue 153. This region contains the sequence Leu-Ser-Leu-Ser-Arg-Phe (residues 108-113), which is strikingly similar to that of the first encephalitogenic determinant. Studies involving the extremely encephalitogenic guinea pig protein demonstrated that virtually all of the activity was recovered in the peptides corresponding to bovine peptides (37-88) and (43-88). These peptides, but not those comprising the remainder of the protein, were active in inhibiting the passive transfer of EAE with lymph node cells from donors immunized with guinea pig spinal cord.
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PMID:The location of regions in guinea pig and bovine myelin basic proteins which induce experimental allergic encephalomyelitis in Lewis rats. 4 54

To induce oral tolerance in multiple sclerosis treatment, we proposed to use the predigested protein of pig spinal cord. The most biologically active composition was obtained from the hydrolysis of an undenaturated homogenate of proteins digested with pepsin. Feeding the rats with our preparation, before or after immunization with MS antigens, strongly reduced development of the experimental autoimmune encephalomyelitis (EAE). The biological results obtained in animals suggest that the developed method of induction of the oral tolerance should be effective in human treatment, at least as a support mechanism in combination with other treatment methods.
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PMID:Protein hydrolysates for oral tolerance. 1121 77