Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Relapsing experimental allergic encephalomyelitis (EAE) was induced in DA rats and the ocular pathologic events were examined at the various phases of the illness. About 80% of EAE rats presented anterior uveitis (AU), even after complete EAE recovery. We studied the phenotype and localization of immunocompetent cells, the major histocompatibility complex (MHC) class I and II antigen expression, as well as the chemokine monocyte chemoattractant protein-1 (MCP-1) appearance. In control animals, there were many glial fibrillary acidic protein (GFAP)(+) cells and OX42(+) cells in the ciliary body, retina, optic nerve and chiasma. Except in retina, we observed constitutive MHC class I and II expression. During the EAE acute phase, there was up-regulation of MHC class II and GFAP antigens in iris, ciliary body, limbus, and optic pathways. MHC class I and ED2 antigens were expressed in meninges and in the prechiasmatic cisterna, by cells which could have a role in immune surveillance. MCP-1 mRNA was highly expressed in optic pathways during the acute phase and the protein was expressed by astrocytes, macrophages, and lymphocytes. During the relapsing phase, MCP-1 was weakly expressed to disappear almost completely during the final recovery phase. The expression of MHC class II on astrocytes was increased during the relapsing and final recovery phase in which the inflammatory lesions persisted. These findings suggest that ocular areas and optic pathways, mainly optic chiasma, are important targets in the relapsing EAE.
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PMID:Distribution in ocular structures and optic pathways of immunocompetent and glial cells in an experimental allergic encephalomyelitis (EAE) relapsing model. 1124 88

In this study, we examined the role of CCL2/MCP-1, CCL3/MIP-1alpha, CCL4/MIP-1beta, and CCL5/RANTES during recurrent anterior uveitis (RAU). LEW rats injected with myelin basic protein (MBP) developed experimental autoimmune encephalomyelitis (EAE) and associated anterior uveitis (AU), which was mediated by CD4(+) T cells. After recovery, rats become resistant to EAE but developed RAU. Rats reinjected with MBP developed RAU without EAE. The chemokines tested were detected in the eye at RAU accelerated onset, increased as the disease progressed, and fell as clinical signs improved. At the same time, in the spinal cords of rats, these chemokines were still detected but at reduced levels. Administration of anti-MIP-1alpha neutralizing antibodies resulted in almost complete suppression of clinical RAU and significant reduction of inflammatory cell recruitment into the iris. Anti-MIP-1beta and anti-MCP-1 antibodies were effective in suppression of RAU but to lesser degree. Treatment with anti-RANTES antibodies was not effective in protecting against the recurrent development of the disease. In the eyes, the message for CCR1 and CCR5 was considerably elevated prior to the onset of AU and decreased after treatment with anti-chemokine antibodies. Our results suggest a crucial role of CCL3/MIP-1alpha in the development of RAU in Lewis rats. In addition, CCL2/MCP-1 and CCL4/MIP-1beta may also play a role in immunopathogenesis of RAU.
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PMID:Crucial role of CCL3/MIP-1alpha in the recurrence of autoimmune anterior uveitis induced with myelin basic protein in Lewis rats. 1214 7

Previous studies have shown that immunization of the Lewis rat with myelin basic protein (MBP), an encephalitogenic antigen derived from the myelin sheath of the CNS, induced both experimental autoimmune encephalomyelitis (EAE) and anterior uveitis (AU). In the current study, we show that a major peptide derived from another encephalitogenic myelin protein-the myelin/oligodendrocyte glycoprotein (MOG35-55)-induced both encephalomyelitis and uveitis in (B6 x SJL) F1 and wt-B6 mice. Pathological studies documented that an anterior uveitis was induced by MOG35-55. A similar disease pattern was induced by either active immunization with peptideMOG35-55 (pMOG35-55) or adoptive transfer of MOG35-55-specific T cells. The induced uveitis persisted for >60 days without remission. Our studies demonstrate for the first time that MOG is uveitogenic in mice that express the H-2(b) genetic background. This new experimental model should provide a useful tool for the study of the pathogenesis of chronic AU and determination of the pathogenic mechanisms by which a large portion of MS patients develops uveitis.
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PMID:Induction of autoimmune encephalomyelitis and uveitis in B6 and (B6 x SJL) mice by peptides derived from myelin/oligodendrocyte glycoprotein. 1241 41

Lewis rats immunized with myelin basic protein (MBP) developed experimental autoimmune encephalomyelitis (EAE) and associated anterior uveitis (AU). Although several cryptic epitopes of MBP have strong encephalitogenic and uveitogenic properties, the peptide corresponding to the MBP residues 1-20 was uniquely capable of inducing AU without EAE. In this study, we showed that acetylation of the N-terminal amino acid did not produce encephalitogenicity, did not enhance uveitogenicity, and did not improve T cell proliferation in Lewis rats. The cytokine production profile induced by MBP(1-20) immunization was consistent with a Th1 response. In MBP-injected rats and in peptide-injected rats, the frequency of the IFN-gamma-secreting cells in MBP(69-89)-stimulated T cells was significantly higher than the frequency of IFN-gamma-secreting cells in MBP(1-20)-stimulated T cells. However, similar numbers of IFN-gamma-producing specific cells were found in the eyes of MBP(69-89) and MBP(1-20) immunized rats. In these rats, the iris-infiltrating cells consisted of a much higher percentage of CD4(+) T cells expressing L-selectin (CD62L) than did those cells found in the spinal cord. The results demonstrate that MBP(1-20) is immunogenic and uveitogenic, although it induced only weak proliferation and weak Th1 reaction. The fact that T cells with the same specificity have different effects on target organs suggested that, in the eye and spinal cord, a distinct mechanism might mediate the recruitment of cells to these organs.
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PMID:Cryptic MBP epitope 1-20 is inducing autoimmune anterior uveitis without EAE in Lewis rats. 1242 4


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