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)

The premise that acute non-fatal viral infections of the central nervous system (CNS) predispose to the subsequent development of chronic immune-mediated neurologic disease was investigated. Adult C57Bl/6 mice inoculated peripherally with 10(4) PFU of the A774 strain of Semliki Forest virus (SFV) develop a transient encephalomyelitis and sporadic (less than 20%) mild symptoms of paralysis with demyelination in the cerebellum from which they recover. Such recovered mice were found to develop signs characteristic of experimental allergic encephalomyelitis (EAE) 2 to 8 wk after either immunization with myelin basic protein (MBP) or receipt of 1 to 2 X 10(7) lymph node cells from MBP-primed syngeneic donors. These two methods of disease induction were unsuccessful when applied to normal B6 mice or those previously inoculated with noninfectious SFV. These findings suggest the possibility that virus-induced damage to CNS tissue may facilitate subsequent priming or clonal expansion of pre-existing myelin-reactive lymphoid cells.
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PMID:Predisposition to EAE induction in resistant mice by prior infection with Semliki Forest virus. 243 86

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

Using lethal irradiation of recipients, adoptive transfer of experimental allergic encephalomyelitis (EAE) into Lewis (LEW) rats using (LEW x PVG/c)F1 (LPVGF1) spleen cells was successfully achieved. Recipient rats usually developed clinical signs of EAE 5 or 6 days after transfer. The EAE was characterized by the presence of a number of petechiae over the spinal cord. Immunohistochemical examination using OX27, a monoclonal antibody specific for RT1.Ac, revealed the localization of transferred F1 (RT1(1/c] cells in the LEW recipients (RT1(1]. Most of the inflammatory cells in the spinal cord lesions were stained positively for OX27, indicating that they were transferred cells. In mild EAE, more W3/25+ cells were found than OX8+ cells. OX8+ cells were predominant in severe EAE, however. Examination of the spleens of rats that developed EAE by OX27 staining revealed that transferred F1 cells gradually increased in number and reached a maximal level on days 5 and 6. In the spleens of rats that received irradiation and transfer but did not develop EAE, few transferred F1 cells were observed. In addition, bromodeoxyuridine (BrdU)-anti-BrdU immunohistochemistry was employed to demonstrate that cell proliferation really takes place in the spleen. It was revealed that the spleens of the recipients of lethal irradiation and F1 cells contained many BrdU+ cells. Because rats given lethal irradiation alone had extremely few BrdU-positive cells in their spleens, labeled cells in the recipients of radiation and transfer originated from transferred F1 cells. Collectively, these findings strongly suggest that transferred cells previously activated in vitro undergo further proliferation in the lymphoid organs of recipients to bring about the development of EAE.
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PMID:Hemorrhagic autoimmune encephalomyelitis induced by adoptive transfer of activated semiallogeneic spleen cells into irradiated rats. 246 Oct 90

Experimental allergic encephalomyelitis (EAE), a T cell-mediated autoimmune disease can be transferred with lymphoid cells from actively immunized rats into naive recipients. In the mouse, previous studies have suggested a role for histamine/serotonin in the development of active EAE. We have found that myelin basic protein-reactive cells transfer a biphasic skin test response to naive rats analogous to what has been described in the mouse contact dermatitis system, where mast cell sensitization by Ag-specific T cell factors is required for the induction of skin test responses. Treatment of cell recipients with the serotonin receptor antagonists, cyproheptadine or methysergide, blocked or significantly reduced the development of EAE. Furthermore, it was found that treatment with cyproheptadine was effective in blocking clinical disease when administered day 3 to day 6 after cell transfer. In contrast, cyproheptadine treatments before induction of paralysis day 0 to 3, failed to alter the course of clinical disease. The inhibitor of mast cell degranulation, proxicromil, was also found to effectively block the elicitation of adoptively transferred EAE and was also found to be effective when administered just before the onset of clinical disease. Reserpine, a compound known to deplete mast cells of vasoactive amines by forcing granule contents into the cytoplasm where they are degraded by cell enzymes, was also effective in blocking both active and adoptively transferred EAE. Disease inhibition was found to be partially reversed with pargyline, an inhibitor of monoamine oxidase. In addition lymphocytes from treated animals were capable of transferring disease to naive recipients and appeared to have normal activity as assessed by Ag-or mitogen-driven proliferation in addition to IL-2 production.
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PMID:The role of mast cells in the elicitation of experimental allergic encephalomyelitis. 246 41

Indomethacin (IM), a specific inhibitor of prostaglandin (PG) synthesis, and PGE2 were studied in terms of their ability to modulate in vitro immune responses associated with experimental autoimmune encephalomyelitis (EAE) in Lewis rats. Lymphoid cells from either the spleens or the draining lymph nodes of myelin basic protein (MBP)-sensitized rats exhibited in vitro immune responses which were enhanced in the presence of IM. Specifically, IM enhanced (i) guinea pig MBP (GPMBP)- and rat MBP (RMBP)-stimulated lymphocyte proliferation, (ii) background proliferation, and (iii) interleukin 2 (IL-2)-stimulated proliferation. Conversely, PGE2 inhibited both GPMBP- and IL-2-stimulated proliferation of MBP-sensitized lymphocytes. Together, these results indicate that PGs secreted by cultured lymphoid cells can directly mitigate MBP- or IL-2-stimulated lymphocyte proliferation. Furthermore, the observation that IM and PGE2 modulate in vitro responses of MBP-specific lymphocytes may provide insight into how the in vivo administration of IM potentiates the severity of EAE (H. Ovadia and P.Y. Paterson, Clin. Exp. Immunol. 49, 386, 1982) and how PGs may be involved in the spontaneous remission of EAE in rats.
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PMID:Indomethacin augments in vitro proliferative responses of Lewis rat lymphocytes to myelin basic protein. Implications for experimental autoimmune encephalomyelitis. 247 May 19

When lymphoid cells from rats recovered from experimental autoimmune encephalomyelitis (EAE) were incubated in vitro for 1 hr with myelin basic protein (BP), then washed and transferred along with anti-BP immune serum to naive recipients, those recipients immediately developed a solid, long-lasting resistance to active induction of EAE. To obtain this high level of suppression, both steps of BP-incubation of cells and transfer of immune serum were found to be essential, i.e., direct transfer of nonincubated cells plus immune serum had no comparable suppressive effect, nor had transfer of BP-incubated cells with nonimmune serum. Specificity of the suppressive effect was indicated by the finding that cells from BP-sensitized donors, incubated with BP, protected against BP-CFA-induced disease but not against disease induced with whole spinal cord homogenate (SCH-CFA). As expected, cells from SCH-CFA-sensitized donors incubated with SCH protected recipients against disease induced with either SCH-CFA or BP-CFA. The suppression appears to act early in the afferent stage of the immune response, since inoculation with incubated cells as little as 24 hr after active challenge was ineffective. There was no suppression of passively induced disease.
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PMID:Immediate, long-lasting suppression of autoimmune encephalomyelitis by cell-bound neuroantigen. 247 40

Inoculation of Lewis rats with live or attenuated (irradiated or paraformaldehyde-fixed) CD4+ encephalitogenic T cells (S1 line) protects the recipients from transferred experimental autoimmune encephalomyelitis (tEAE) induced by S1 cells. A CD8+ T lymphocyte population specifically activated against the EAE-inducing S1 cells can be readily isolated from the lymphoid organs of pretreated animals. We show, in the present study, that encephalitogenic T cell lines derived from Lewis rats differ in their ability to induce resistance against tEAE in vivo and to stimulate CD8+ cell proliferation in vitro. We also demonstrate that the S19 line of encephalitogenic T cells, in combination with myelin basic protein (MBP), can stimulate CD8+ cell proliferation in vitro. The CD8+ cells generated in this way strongly suppress MBP-specific T cell proliferation in vitro. This combined effect of T cells and MBP was also evident in vivo. Neither S19 cells nor MBP alone induced resistance against S19-mediated tEAE, rather coinjection of these cells and MBP was required. Our results suggest that resistance to EAE is mediated by distinct populations of encephalitogenic T cells that activate Ts cells through different mechanisms. In some instances, both autoreactive T cells and their relevant autoantigen(s) may be needed to activate Ts cells in vivo.
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PMID:Functional heterogeneity among CD4+ encephalitogenic T cells in recruitment of CD8+ T cells in experimental autoimmune encephalomyelitis. 247 27

The effect of timing of a local host-versus-graft reaction on the induction of acute experimental allergic encephalomyelitis (EAE) was studied in guinea pigs. 20 x 10(7) gamma-irradiated allogeneic cells injected 4 days after encephalitogenic challenge resulted in the development of EAE with an earlier onset, an increased delayed-type hypersensitivity (DTH) response and an increase in lymphoid cell infiltration in the spinal cord. Challenge with allogeneic cells on days -4 and -7, however, produced a delay in onset and a protracted course of disease, with 30-40% of the animals recovering. Evidence of disease was confirmed histologically.
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PMID:Modulation of experimental allergic encephalomyelitis by a host-versus-graft reaction: a clinicopathological study. 247 57

Adoptive transfer of experimental allergic encephalomyelitis (EAE) is enhanced after in vitro culture of myelin basic protein (BP)-sensitized lymphoid cells with BP. Addition of lipopolysaccharide (LPS) to the culture further augments transfer of EAE to a level 5 times greater than that achieved with cells activated only with BP. Neither the proliferative response of a BP-specific cell line nor the production of IL-2 by BP-sensitized lymphoid cells in response to BP was augmented by the addition of LPS to the culture. Augmentation of EAE was also observed if recipients received simultaneous injections of BP-sensitized lymph node cells (BP/LNC) cultured with BP (BP-activated) and normal spleen cells cultured independently with LPS (LPS/Spl-C). To analyze the effect of contact between these two cell populations in vivo, we mixed the two cell populations in vitro at reduced cell concentrations. When BP-activated BP-LNC were mixed with LPS-Spl-C in vitro, a marked synergistic proliferative response was observed. Irradiation of BP-activated BP/LNC abrogated this synergistic response, whereas irradiation of LPS/Spl-C did not, suggesting that the proliferating population was in the BP/LNC and that the LPS/Spl-C enhanced their proliferation. These results indicate that LPS exerts its effect through BP-nonspecific cells and that these cells enhance transfer of EAE by augmenting the proliferation of the BP-specific cells in vivo after transfer.
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PMID:LPS augments adoptive transfer of experimental allergic encephalomyelitis in the Lewis rat. 248 79


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