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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental autoimmune encephalomyelitis (EAE) is a T cell-mediated autoimmune disease inducible in rodents by immunization of brain-specific antigens such as myelin basic protein (MBP). It is also well known that various strains of rats differ in their susceptibility to EAE upon active immunization. To elucidate the immune mechanisms of susceptibility and resistance to EAE, we first examined the T cell repertoire for MBP using thymectomized chimeras that possessed thymuses from EAE-susceptible (LEW) or EAE-resistant (BM) strains. It was revealed that T cell specificity of these chimeras was skewed toward that of the grafted thymus. Very interestingly, the chimeras bearing thymuses from the resistant strain developed severe EAE, keeping a hole in the encephalitogenic 68-88 sequence of MBP. These findings suggest that the strain-specific T cell repertoire itself is not involved in the regulation of EAE susceptibility. Furthermore, the analysis of the chimeras reconstituted with F1 T cells and marrow cells from various strains indicates that the major histocompatibility complex (MHC) molecules expressed on accessory cells primarily determine susceptibility or resistance to EAE. We finally showed, using various inbred and congenic rats carrying RT1l or RT1n, that susceptibility to EAE of rats carrying RT1l is heavily influenced by the background genes, whereas resistance to EAE of rats carrying RT1n is primarily regulated by the MHC molecules expressed on accessory cells without influence of the background genes.
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PMID:Analysis of the T cell repertoire for myelin basic protein in thymus-grafted and other types of chimera: evidence that major histocompatibility complex molecules on accessory cells rather than T cell specificity mainly regulate susceptibility to autoimmune encephalomyelitis. 169 40

Effective T cell vaccination against experimental autoimmune diseases involves treatment with activated, autoimmune T lymphocytes. The present study was undertaken to learn whether antigen-specific T cells present in low frequency could be selected in vitro without using the specific antigen. The rat models of adjuvant arthritis and experimental autoimmune encephalomyelitis were investigated using proliferation assays and limiting dilution techniques to quantify the changes in reactivity of a heterogenous population of lymphocytes to the relevant antigen. Stimulation with concanavalin A for 2 d and then culture in IL-2-containing medium led to a substantial increase in the activity and frequency of the specific autoimmune T cells. Enrichment of antigen-specific T cells could be demonstrated using lymph node, spleen, or peripheral blood lymphocytes, from rats late in the course of disease. The effect was not evident in lymphocytes from the thymus. These results are relevant to the clinical application of T cell vaccination and to investigation of self-antigens in autoimmune disease.
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PMID:Clinical modeling of T cell vaccination against autoimmune diseases in rats. Selection of antigen-specific T cells using a mitogen. 211 Jan 91

Three categories of cell lines are described with respect to their activity in binding Theiler's murine encephalomyelitis virus (TMEV). High, medium and low densities of viral receptors can be detected on cell lines from different species and origins by using an immunological binding assay. Nevertheless, TMEV acts as a fastidious virus that only infects a few cell types productively. No correlation between virion binding and degree of permissiveness to infection could be detected. The presence of viral receptors in both susceptible and resistant strains of mice seemed to have a widespread tissue distribution, the thymus being an exception. When primary cerebral cultures, enriched in neurons, astrocytes or oligodendrocytes, were checked in the immunological assay, a higher density of viral receptors was detected in the neuronal population. The number of virus-binding sites in the BHK-21 cell line is reported here to be 5 x 10(3) per cell; approximately 15 x 10(3) and 2.5 x 10(3) are the estimates of binding sites per cultured neuron and macroglial cell, respectively.
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PMID:Theiler's murine encephalomyelitis virus-binding activity on neural and non-neural cell lines and tissues. 227 88

Effector cells mediating experimental allergic encephalomyelitis (EAE) were recovered from the thymus glands and spinal cords of Lewis rats immunized with myelin basic protein (BP) and complete Freund's adjuvant (CFA), as demonstrated by adoptive transfer to syngeneic recipients following in vitro activation with BP. The thymic effector cells (TCs) were lymphoblasts. Sequential transfer studies suggested that the effector TCs probably recirculated back to the thymus from the periphery. The transfer of EAE with cells derived from the spinal cords of paralyzed donors indicates that disease-inducing effector cells are present in the target organ.
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PMID:Autoimmune effector cells. VII. Cells isolated from thymus and spinal cord of rats with experimental allergic encephalomyelitis transfer disease. 241 87

Chronic relapsing experimental allergic encephalomyelitis was induced in SJL mice by adoptive transfer of long-term cultured T cell lines. The T cells which were activated with myelin basic protein (MBP) derived from various species, all induced chronic relapsing experimental allergic encephalomyelitis with a similar high incidence. During the relapsing stage, lymphocytes obtained from the spleen responded well to MBP and were capable of transferring experimental allergic encephalomyelitis, whereas thymus lymphocytes did not respond to MBP. There was no difference in the proliferative response of splenocytes to MBP when splenocytes were isolated either from mice with clinical relapse or from mice that did not relapse. Pathological examination revealed a transient appearance of inflammatory cells during the acute stage. Similar cell infiltrates were also observed at the relapsing stage. The I-region associated (Ia) antigens appeared on vessels and astrocytes in the acute inflammatory lesions which coincided with the appearance of inflammatory cell infiltrates. Ia antigen expression diminished with the disappearance of inflammatory cells. During the relapsing stage, the Ia antigens were also expressed on the vessels and astrocytes in the fresh lesions. Our data indicate that MBP-reactive T cells persist at least in the spleen, for a long time. They may be reactivated by certain mechanisms probably in the central nervous system associated with the Ia-antigen expression, which facilitates the effector phase again. The initial event that triggers the Ia-expression is not known as yet.
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PMID:Ia expression in chronic relapsing experimental allergic encephalomyelitis induced by long-term cultured T cell lines in mice. 241 66

The relationship between surface marker expression and encephalitogenicity of lymphocytes from various lymphoid organs of Lewis rats was studied. The encephalitogenicities after culture with BP were spleen cells greater than lymph node cells much greater than thymus cells, in this descending order. The cells from every lymphoid organ proliferated significantly in response to BP. In spleen and lymph node cells, the expression of W3/25 and OX-3 molecules on T cells increased markedly after culture with BP, but the expression of OX-19 or OX-8 molecules did not change significantly. The up-regulations of W3/25 and OX-3 molecules were more pronounced in spleen cells than in lymph node cells. Thymus cells also showed a significant increase in the W3/25 molecule after the culture with BP. Therefore, T cells from all the lymphoid organs showed a selective up-regulation of the W3/25 molecule after culture with BP, and the degree of the up-regulation seems to correspond to the encephalitogenic potency in vivo. Since the W3/25 molecule apparently plays a direct role in the effector phase of experimental allergic encephalomyelitis (EAE) by enhancing BP-reactive T cell/antigen-presenting cell interaction in the central nervous system, the up-regulation on BP-cultured T cells may strengthen interaction with the class II major histocompatibility complex molecule on antigen-presenting cells, and therefore, contribute to the efficient transfer of EAE.
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PMID:Relationship between surface marker expression and encephalitogenic potency of BP-cultured lymphocytes. 244 77

The immune response measured by the level of specific anti-myelin antibodies and inflammatory process indicator-haptoglobin, were studied in chickens immunized with myelin basic protein (MBP). The histopathological changes in lymphoid organs were also investigated. The occurrence of specific anti-myelin antibodies was shown in sera of immunized animals. High level of antibodies was found in IgG class. The concentration of anti-myelin antibodies in the remaining immunoglobulin classes showed different levels. High concentration of haptoglobin (up to 2 g/l) was regularly noted in the course of allergic encephalomyelitis. All the above parameters were also evaluated in the course of experimental therapy with thymus factor X (TFX). This preparation distinctly reduced haptoglobin level in serum and had only slight effect on humoral immunity. In the course of inflammatory process plasmatic cells stimulation in the spleen was observed microscopically: this was even enhanced by the thymus hormone. The lymphoid system did not undergo any significant changes. The Harder's gland did not seem to have any influence upon the induction or therapy of MBP-induced inflammation.
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PMID:Thymus factor X (TFX) in modulation of immune and inflammatory response in chickens immunized with myelin basic protein (MBP). 245 9

We previously reported the presence of suppressor cells in Lewis rats at the very time of spontaneous recovery from experimental autoimmune encephalomyelitis. As these 'recovery-associated' suppressor cells might be implicated in the self-cure process, we investigated their specificity on the in vitro lymphoproliferative responses of a T cell line specific for myelin basic protein (MBP). We report now that these suppressor cells found in the thymus are specific for MBP, and not for T cell receptors, contrasting with the 'post-recovery' suppressor cell specificity reported by others. Furthermore, they do not recognize the encephalitogenic peptide 71-84, suggesting that their specificity involves an epitope outside (or partially out of) the encephalitogenic sequence.
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PMID:Regulation of experimental autoimmune encephalomyelitis. Specificity of the 'recovery-associated' suppressor cells. 246 12

A feature common to many animal models of autoimmune disease, for example, experimental allergic encephalomyelitis, experimental autoimmune myasthenia gravis and collagen-induced arthritis, is the presence of self-reactive T cells in healthy animals, which are activated to produce disease by immunization with exogenous antigen. It is unclear why these T cells are not deleted during ontogeny in the thymus and, having escaped tolerance induction, why they are not spontaneously activated by self-antigen. To investigate these questions, we have examined an experimental model in which mice are tolerant to an antigen despite the presence of antigen-reactive T cells. We find that the T cells that escape tolerance induction are specific for minor determinants on the antigen. We propose that these T cells evade tolerance induction because some minor determinants are only available in relatively low amounts after in vivo processing of the whole antigen. For the same reason, these T cells are not normally activated but can be stimulated under special circumstances to circumvent tolerance.
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PMID:How some T cells escape tolerance induction. 247 88

Experimental autoimmune encephalomyelitis (EAE) is a cell-mediated autoimmune disease of the central nervous system that has been extensively studied in the rat. The Lewis rat is highly susceptible to the induction of EAE, while the Lewis resistant (LeR) rat is known to be resistant. In this paper, we demonstrate that the LeR rat, which was derived from the Lewis strain by inbreeding of fully resistant animals, is histocompatible with the Lewis strain. Radiation chimeras, a tool for distinguishing between immunologic and nonimmunologic resistance mechanisms, were utilized to analyze the cellular mechanisms involved in genetic resistance to EAE. By transplanting bone marrow cells from LeR rats into irradiated Lewis recipients, Lewis rats were rendered resistant to EAE induction. Likewise, transplanting Lewis bone marrow cells into irradiated LeR recipients rendered LeR rats susceptible. Mixed lymphoid cell chimeras using bone marrow, spleen, and thymus cells in Lewis recipient rats revealed individual lymphoid cell types and cell interactions that significantly affected the incidence and severity of EAE. Our results suggest that LeR resistance is mediated by hematopoietic/immune cells, and that cells located in the spleen appear to play a critical role in the resistance/susceptibility to EAE induction. Depletion of splenic adherent cells did not change the patterns of EAE resistance. In vivo cell mixing studies suggested the presence of a suppressor cell population in the LeR spleen preparations which exerted an inhibitory effect on Lewis autoimmune responses. Thus, the mechanism of LeR resistance appears to be different from that in other EAE-resistant animals.
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PMID:Genetic resistance in experimental autoimmune encephalomyelitis. I. Analysis of the mechanism of LeR resistance using radiation chimeras. 252 17


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