Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004364 (autoimmune disease)
 24,845 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It was confirmed that experimental autoimmune encephalomyelitis EAE, could be induced in SJL/J mice with mouse spinal cord homogenate. It was shown that induction of EAE in mice was critically dependent on the concentration of pertussis vaccine. The encephalitogen present in mouse brain was the basic protein of myelin. The smaller form of the mouse and rat basic proteins induced EAE; thus the mouse like the rat responds to determinants other than the "tryptophan region," which induced EAE in guinea-pigs. Mice with EAE developed a cell-mediated immune response to myelin basic protein, as judged by inhibition of peritoneal cell migration. However, levels of antibody to mouse basic protein were low, as judged by radioimmunoassay. The establishment of this autoimmune disease model in the mouse will allow the application of well established techniques for the analysis of the immunologic mechanisms leading to disease manifestation.
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PMID:Experimental autoimmune encephalomyelitis in mice: immunologic response to mouse spinal cord and myelin basic proteins. 4 66

Lymph node cells (LNC) from Lewis rats rendered unresponsive to experimental allergic encephalomyelitis (EAE) by pretreatment with myelin basic protein markedly suppressed clinical (but not histologic) EAE in normal recipients later challenged with an encephalitogenic emulsion. Unresponsiveness was immunologically specific, and required viable LNC; serum transfer was ineffective. These findings suggest that suppressor cells exert control over this autoimmune disease.
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PMID:Suppressor cell control of unresponsiveness to experimental allergic encephalomyelitis. 5 Mar 70

The immunopathogenesis of experimental allergic encephalomyelitis (EAE) is reviewed with special focus on the role of central nervous system fibrin deposition in the inflammatory cascade characterizing this autoimmune disease. Among rats sensitized to whole spinal cord or myelin basic protein of either guinea pig or bovine origin, there is a striking degree of concordance of perivascular fibrin deposits and occurrence of clinical paralytic signs. Neither paralytic signs nor fibrin deposition are temporally related to development of perivascular cellular infiltrates. Rats sensitized to neuroantigen and treated with ancrod, a polypeptide derived from the venom of Agkistrodon rhodostoma, develop profound hypofibrinogenemia, have a marked inhibition of fibrin deposition, and often exhibit no paralytic signs whatsoever. In contrast, cellular infiltrates are not demonstrably influenced by ancrod treatment. Activation of the clotting cascade at loci of developing immune injury of nervous tissue appears to result from and lead to increasing neurovascular permeability and accumulation of edema fluid. Distention of the extracellular space in central and peripheral nervous system tissues by edema fluid appears to be directly responsible for clinical abnormalities characterizing EAE in rats. Cellular infiltrates, on the other hand, appear to be an independent immune response to neuroantigenic sensitization.
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PMID:Experimental allergic encephalomyelitis: role of fibrin deposition in immunopathogenesis of inflammation in rats. 6 95

A modified electrophoretic mobility (EM) test was performed in 150 children to examine their lymphocyte sensitization to myelin basic protein (encephalitogenic factor). Measurements in the cytopherometer were facilitated by using devitalized sheep erythrocytes as indicator particles instead of macrophages. A significant decrease in EM was found in 29/30 children with acute lymphoblastic leukaemia and in 67/75 children with solid tumours, thus giving a false negative rate in malignant disease of 9/105=8-6%, as compared to 6 false positives among 45 children with non-malignant disorders; 5 of the later "false/positive" 6 patients had autoimmune disease. Results of the EM test in the children with leukaemia were compared with those in 9 patients with non-Hodgkin's lymphoma and 2 with Hodgkin's disease at different stages, but no striking change was seen between different diseases, or after cessation of long-term immunosuppressive chemotherapy. Percentage of "slowing" ranged from 4 to 30%. These results indicate that patients with lymphoid malignancies still have lymphocytes which had been sensitized by a common antigen of the malignant cell clone at the beginning of the disease. The EM test, furthermore, could serve as an additional diagnostic aid in differentiating benign from malignant masses in the abdomen, extremities or intracranial disease.
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PMID:Lymphocyte sensitization in childhood solid tumours and lymphoblastic leukaemia, measured by electrophoretic mobility test. 6 84

The hemagglutinating antibody responses of Lewis rats with experimental allergic encephalomyelitis (EAE) and of rats rendered unresponsive to this autoimmune disease by pretreatment with myelin basic protein (BP) were compared. Most tolerant animals produced low levels of hemagglutinating antibody. Similarly, most rats with EAE also produced anti-BP antibodies. We were unable to correlate hemagglutinin production or titer with protection against disease. Hemagglutination inhibition (HAI) studies reveal cross-reactivity between rat, guinea pig and bovine BP. HAI studies with BP-derived peptides suggest that at least three distinct antibody-binding determinants exist in the BP molecule, and that individual inbred Lewis rats respond differently with respect to antibody production to these sites.
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PMID:Antibody response to myelin basic protein: comparisons between Lewis rats with experimental allergic encephalomyelitis, and tolerant rats. 7 24

Cellular transfer of experimental autoimmune encephalomyelitis (EAE) was effected in mice with lymph node and spleen cells from appropriately immunized donors. In contrast to lymphoid cells, immune serum did not transfer this autoimmune disease nor did serum have any facilitating or inhibitory effect on the capacity of lymphoid cells to transfer EAE. Transfer of EAE was effected in normal mice, lightly irradiated (350 rad) and lethally irradiated (850 rad) and bone marrow-protected mice, but not in mice which had been given 850 rad total-body irradiation. There was a striking augmentation of severity of transferred EAE in the lightly irradiated recipients, possibly attributable to selective radiosensitivity of suppressor T cells. Cell-mediated immunity but not circulating antibody to basic protein of myelin was demonstrated in recipients with transferred EAE. The immune lymphoid cells responsible for transfer of EAE were T lymphocytes. Thus transfer was successful after passage of sensitized cells through anti-immunoglobulin columns and was abrogated following treatment with anti-Thy-1 serum and complement. Neonatally thymectomized mice failed to develop either EAE, cell mediated immunity or humoral antibody against myelin basic protein (BPM). Inhibition of EAE and immune responsiveness was solely due to the removal of the source of thymus lymphocytes, because reconstitution of neonatally thymectomized mice with T lymphocytes completely restored these functions. It is concluded that T lymphocytes are required for the production and adoptive transfer of EAE, for the development of cell-mediated immunity to BPM and for the production of antibody to BPM.
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PMID:T cell necessity in the pathogenesis of experimental autoimmune encephalomyelitis in mice. 108 43

Lewis rats immunized with T cell receptor (TCR) variable region peptide V beta 8 in complete Freund's adjuvant (CFA) were protected against experimental autoimmune encephalomyelitis (EAE) induced with myelin basic protein in CFA, although variable protection was also observed in rats injected with control peptide in CFA, or CFA alone. However, this adjuvant-mediated protection could be avoided by immunizing with TCR peptide in incomplete adjuvant (IFA). Clinical, but not histologic EAE was suppressed in rats given V beta 8 peptide in IFA, whereas control animals injected with V beta 14 peptide in IFA, or IFA alone developed severe clinical EAE. Anti-V beta 8 antibodies were present in the sera of all V beta 8-treated rats. These findings lend support to the hypothesis that autoimmune disease can be suppressed by inducing an immune response against the TCR-idiotope of autoreactive T cells.
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PMID:Studies of V beta 8 T cell receptor peptide treatment in experimental autoimmune encephalomyelitis. 137 25

The efficacy of antigen-specific immunoregulation as a treatment for the efferent limb of an autoimmune disease was tested in a rat model of adoptive experimental autoimmune encephalomyelitis (EAE). Lewis rats receiving 4-5 x 10(7) guinea pig (GP) myelin basic protein (MBP)-activated lymph node T cell blasts from GPMBP/CFA sensitized donors routinely show clinical signs of disease 5-6 days post transfer. Intravenous injection of GPMBP coupled to syngeneic splenocytes using the chemical cross-linker carbodiimide was effective in completely abrogating the expression of clinical EAE in rats that received MBP-specific T cells 2 days previously. Partial inhibition was also observed in rats injected as early as day 0 (the same day as MBP-specific T cell transfer) and as late as 1 day prior to the onset of clinical signs (days 4-5 post transfer). Unresponsiveness was shown to be dose-dependent, dependent on the route of injection of the neuroantigen-coupled splenocytes, and was antigen-specific. Splenocytes coupled with GP or rat MBP (which are identical within the major encephalitogenic GP68-86 Lewis rat determinant with the exception of the residue at position 80) were equally efficient at eliminating disease expression in recipients of GPMBP-specific T cells. In contrast, splenocytes coupled with bovine or rabbit MBP (which differ significantly from GPMBP within the 68-86 region) had no inhibitory effect. The antigen specificity of the tolerance induction was also illustrated by the fact that splenocytes coupled with GP68-86, but not those coupled with the truncated GP68-84 peptide, induced profound unresponsiveness. Interestingly, de novo antigen processing by the antigen-coupled cells did not appear to be necessary as the inclusion of antigen processing inhibitors had no effect on inhibition of disease. However, the use of the carbodiimide coupling reagent was critical for the induction of unresponsiveness as essentially equivalent amounts of 125I-labelled MBP were bound in its presence or absence, but only splenocytes incubated in the presence of both MBP and carbodiimide inhibited clinical expression of disease. Antigen-specific tolerance is thus an effective means of inhibiting expression of clinical disease in the rat EAE model, and a powerful tool for determining the fine epitope specificity of encephalitogenic T cells.
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PMID:Antigen-specific inhibition of the adoptive transfer of experimental autoimmune encephalomyelitis in Lewis rats. 137 53

Immunization with myelin basic protein (MBP) induces experimental allergic encephalomyelitis (EAE), a prototype of CD4+ T-cell mediated autoimmune disease. In rodents, MBP-reactive T-cell clones are specific for a single, dominant determinant on MBP and use a highly restricted number of T-cell receptor genes. Accordingly, EAE has been prevented by various receptor-specific treatments, suggesting similar strategies may be useful for therapy of human autoimmune disease. Here we report that in (SJL x B10.PL)F1 mice, immune dominance of a single determinant, MBP:Ac1-11, is confined to the inductive phase of EAE. In mice with chronic EAE, several additional determinants of MBP in peptides 35-47, 81-100 and 121-140 recall proliferative responses. Most importantly, reactivity to the latter determinants was also detected after induction of EAE with MBP peptide Ac1-11 alone; this demonstrates priming by endogenous MBP determinants. Thus, determinants of MBP that are cryptic after primary immunization can become immunogenic in the course of EAE. Diversification of the autoreactive T-cell repertoire due to 'determinant spreading' has major implications for the pathogenesis of, and the therapeutic approach to, T-cell driven autoimmune disease.
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PMID:Spreading of T-cell autoimmunity to cryptic determinants of an autoantigen. 137 68

Experimental allergic encephalomyelitis (EAE) is an autoimmune disease characterized by inflammation and demyelination in the central nervous system (CNS). Administration of transforming growth factor-beta (TGF-beta) has been shown to inhibit EAE. In this study, the possible role of endogenous TGF-beta in the regulation of relapsing EAE produced by the transfer of myelin basic protein-specific T cell lines was assessed. Although TGF-beta is not present in the normal CNS, this cytokine was detected by immunohistology in areas of central nervous system inflammation in both acute and chronic disease. The administration of anti-TGF-beta at the disease onset led to a worsening of the clinical course of EAE and more extensive pathological lesions. These findings provide direct evidence for a role of endogenous TGF-beta in the remissions seen in chronic relapsing EAE.
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PMID:Evidence of endogenous regulatory function of transforming growth factor-beta 1 in experimental allergic encephalomyelitis. 137 98


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