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)

Neuropathological studies were performed in order to investigate experimental allergic encephalomyelitis induced by long-term cultured T cell lines and clones specific for myelin basic protein, which were established from SJL/J and DDD/1 mice. All antigen-activated T line or clone cells induced similar disease in euthymic and athymic mice with a common I-A haplotype. The lesion was characterized by perivascular and parenchymal infiltration of mononuclear cells with abundant polymorphonuclear cells located mainly in the lower spinal cord. Axons were severely affected and decreased in number. However, demyelination was present in all cases and was especially marked when recipient mice were: given whole-body X-ray irradiation, I-A compatible other strains, or were congenitally athymic. Topographically, demyelinated axons were most prominent in the root exit and entry zones of the lower spinal cord. Repeated transfer or relapse did not seem to be the factor responsible for enhancing demyelination. We conclude that: inflammation with axonal damage is the main feature of murine experimental allergic encephalomyelitis induced by myelin basic protein-specific T cell lines and clones, demyelination definitely occurs under certain conditions and in certain areas especially at the root exit and entry zones in nude mice, and a single T cell clone induces experimental allergic encephalomyelitis lesions associated with demyelination without the aid of interaction with another recipient-derived T cell population.
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PMID:Demyelination induced by T cell lines and clones specific for myelin basic protein in mice. 243 89

The role of T-T cell interactions in the clinical course of acute experimental allergic encephalomyelitis (EAE) in mice was investigated. Myelin basic protein (MBP)-reactive and encephalitogenic T cell clones were established from long-term lines derived from susceptible strain SJL/J mice and resistant strain DDD/1 mice. The lines and clones from DDD/1 mice were obtained by immunization of congenitally athymic mice of DDD/1 origin, which had been reconstituted with syngeneic Lyt-2+-depleted splenic T cells. The clones derived from both strains bore surface phenotypes of Lyt-1+, 2- and L3T4+, and proliferated well in response to rat, rabbit, bovine, and guinea pig MBP in the presence of antigen-presenting cells with I-As. Passive EAE could be induced in syngeneic normal recipients by these clones as well as by the lines from which the clones were derived. The clinical features of the clone-induced EAE were essentially the same as those of the line-induced EAE. Furthermore, DDD/1 athymic recipients developed signs of acute EAE by the adoptive transfer of I-A-compatible syngeneic and allogeneic T cell clones, in which there was no significant difference in time of onset, maximum severity, or prognosis. These results indicate that the entire clinical course of acute EAE can be elicited by a single population of MBP-reactive T cells in the absence of the thymus and other populations of primed or unprimed T cells.
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PMID:Studies of experimental allergic encephalomyelitis by using encephalitogenic T cell lines and clones in euthymic and athymic mice. 348 35

The expression of acute experimental autoimmune encephalomyelitis (EAE) in mice is controlled by several dominant genes, H-2 and histamine sensitization genes. SJL/J and SWR/J, which are H-2s and H-2q, respectively, are susceptible to EAE and sensitive to Bordetella pertussis histamine-sensitizing factor (HSF), which produces a vasoactive amine hypersensitivity. Other H-2s or H-2q strains such as A.SW, B10.Q and several others do not develop acute EAE and are not sensitive to B. pertussis HSF. One strain tested, DDD (KsIsD?) is HSF sensitive but does not develop EAE (presumably because it lacks the appropriate responder H-2 haplotype). However, F1 hybrids between B10.S and DDD are sensitive to HSF and develop EAE. The induction and effector phases of acute EAE are apparently controlled by the combination of H-2 and HSF genes. A combination of the correct H-2 hapotype and histamine sensitivity is required for the development of acute EAE.
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PMID:Acute autoimmune encephalomyelitis in mice. II. Susceptibility is controlled by the combination of H-2 and histamine sensitization genes. 680 29