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)

Lewis rats are susceptible to experimental autoimmune encephalomyelitis (EAE), and their T lymphocytes recognize epitopes in the 68-88 sequence of guinea pig myelin basic protein (BP). BN rats are resistant to EAE, and their T lymphocytes recognize epitopes outside of the 68-88 sequence, probably in the 43-67 portion of BP. To investigate the influence of the genome of antigen-presenting cells (APC) on the dominance of BP epitopes for T lymphocyte lines, we selected anti-BP lines from (Lewis X BN)F1 rats by using the APC of Lewis, BN, or F1 origin. We now report that the F1/Lewis and F1/F1 lines recognized the 68-88 epitopes and were highly encephalitogenic in F1 rats, whereas the F1/BN line recognized the 43-67 epitopes and was only weakly encephalitogenic. Thus, the genotype of the APC can influence the immunologic dominance for T lymphocytes of BP epitopes, and this dominance in turn can influence the expression of disease.
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PMID:Experimental autoimmune encephalomyelitis mediated by T lymphocyte lines: genotype of antigen-presenting cells influences immunodominant epitope of basic protein. 241 8

A T lymphocyte line, BP-1, expressing the T helper phenotype was selected from Lewis rats immunized with guinea pig myelin basic protein (GP-BP) in complete Freund's adjuvant (CFA). The BP-1 line responded specifically to GP-BP but not to PPD after the first round of selection, and responded to rat but not human or bovine BP. When injected i.p. into histocompatible Lewis or F1 (Lewis X P2) recipients, the BP-1 line induced both clinical signs of experimental autoimmune encephalomyelitis (EAE) and delayed type hypersensitivity (DTH) reactions in ears challenged intradermally with GP-BP but not PPD. The severity of clinical signs and the degree of ear swelling were dependent on the dose of BP-1 cells injected. Both activities were detectable with as few as 0.1 X 10(6) BP-1 line cells and required prior activation of the line cells with GP-BP presented by accessory cells. Lewis rats that had recovered from EAE induced by injection of GP-BP in CFA were more susceptible than naive rats to BP-1 line-mediated disease, requiring as few as 0.03 X 10(6) line cells. Clinical EAE and DTH could be serially transferred into F1 (Lewis X P2) recipients with BP-1 cells and back to nonirradiated Lewis parents with activated splenocytes, suggesting that BP-1 cells persist in recipient rats. These results demonstrate the potent biologic activities of an autoreactive BP-specific T lymphocyte line. This line possesses properties similar to BP lines described previously as well as to culture-conditioned splenic T effector cells; thus, the data presented here bridge the gap between these two approaches for studying T effector lymphocyte functions.
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PMID:A myelin basic protein-specific T lymphocyte line that mediates experimental autoimmune encephalomyelitis. 258 32

Clinical resistance to the induction of experimental allergic encephalomyelitis was observed in a closed colony of Lewis (designated Le-R) rats. Disease susceptibility in randomly bred animals appeared to increase with increasing age. In the small group of young Le-R rats, which were susceptible, disease onset was delayed, severity of symptoms was reduced, and duration of clinical signs was abbreviated compared to conventional Lewis rats. The severity of histologic neural tissue lesions correlated with clinical observations. Breeding experiments indicated that most Le-R rats were resistant to disease induction regardless of whether their ancestors had been selected for susceptibility or resistance. The F3 generation of resistant lineage was uniformly resistant at all ages tested. Virtually all (Lewis X Le-R)F1 rats of either sex were resistant when challenged at 7-8 wk of age indicating that resistance was a dominant autosomal trait. Approximately half of (F1 X Lewis) backcross rats developed paralytic EAE whereas one-fourth were entirely resistant, suggesting that disease resistance may be mediated by one or two genes. Le-R rats shared at least some of the Lewis rat major histocompatibility antigens. Resistance apparently did not reflect a nonspecific impairment of cellular immune responsiveness. Le-R rats, which had been challenged with myelin basic protein, developed antigen-reactive cells specific for basic protein or its encephalitogenic fragment. Spleen cells obtained from basic protein-sensitized Le-R rats did not adoptively transfer disease into Lewis rats. In contrast, spleen cells obtained from basic protein-sensitized Lewis rats readily transferred disease into both Lewis and Le-R recipients. These data suggest that disease resistance may be a result of an immunologic deficit (or suppressor cell activity) expressed during the differentiation of antigen-reactive cells into disease-inducing effector cells.
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PMID:Genetic resistance to the induction of experimental allergic encephalomyelitis in Lewis rats. I. Genetic analysis of an apparent mutant strain with phenotypic resistance to experimental allergic encephalomyelitis. 616 Dec 6