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

In old BALB/c mice susceptibility to experimental allergic encephalomyelitis (EAE) with bovine proteolipid apoprotein (PLP) is reduced significantly. Eleven of 21 8-week BALB/c mice developed clinical signs of EAE following injection of PLP but only two of 18 12-month BALB/c mice and one of 19 24-month BALB/c mice showed clinical signs of EAE. Susceptibility to EAE induced by either PLP or bovine myelin basic protein (MBP) also was reduced in old SJL mice. However, the aging process had no effect on the clinical signs of EAE in both strains, if EAE appeared. Some old BALB/c mice developed histologic EAE with significant demyelination without clinical signs. Lymphocyte proliferative response to mitogens and antigens, and interleukin-2 (IL-2) production, also were depressed in the aged mice (24-month BALB/c and 18-month SJL) probably due to the functional defect of T cells, since the function of macrophages as antigen-presenting cells was not affected in the old mice. PLP-sensitized spleen cells (SPC) from 8-week mice were able to adoptively transfer EAE to young and aged recipients. PLP-sensitized T cells from 8-week mice, reconstituted with young or old monocytes, also were able to transfer EAE into young mice. In contrast, spleen cells from aged mice did not induce EAE, so the reduction of EAE susceptibility was mainly explained by the failure of T cell activity. This T cell defect was not restored by exogenous IL-2.
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PMID:Studies of experimental allergic encephalomyelitis in old mice. 169 15

We investigated in mice strain differences in induction of experimental allergic encephalomyelitis by proteolipid apoprotein and studied encephalitogenic determinants. SJL/J, C3H/He, CBA/J and A/J mice were high responders, BALB/c and AKR/J mice were moderately susceptible, and DBA/2, B6 and congenic strains of B10 background were low responders. Synthetic peptide 136-150 was encephalitogenic for SJL/J mice, and 215-232 was encephalitogenic for C3H/He mice. These encephalitogenic derterminants are present in the extracellular portion of proteolipid apoprotein in myelin.
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PMID:Susceptibility to proteolipid apoprotein and its encephalitogenic determinants in mice. 170 4

This study was aimed at restoring decreased T-cell functions and reduced susceptibility to proteolipid apoprotein (PLP) induced-experimental allergic encephalomyelitis (EAE) in old mice with thymic hormones. Thymosin fraction 5 (TF-5) and serum thymic factor (FTS) had no significant in vitro and in vivo effect on proliferative responses to PLP and concanavalin A (Con A), and on EAE induction in young and old mice. These results suggest that decreased T-cell functions cannot be restored by these thymic hormones tested.
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PMID:Effect of thymic hormones on induction of experimental allergic encephalomyelitis in old mice. 225 3

The role of myelin proteolipid apoprotein (PLP) in the central nervous system (CNS) immune response of rabbits has been investigated by analyzing the immunopathology of chronic experimental allergic encephalomyelitis (EAE) induced by sensitization with PLP. Clinical disease occurred in seven out of nine rabbits sensitized with bovine PLP and monitored for up to 6 mo. Positive delayed hypersensitivity skin test reactions to PLP occurred in all but one of the PLP-sensitized animals. All PLP-sensitized animals had meningeal and CNS parenchymal inflammation that correlated with disease severity. Serial blood samples were stained with a panel of antibodies to rabbit T and B cells, as well as Ia, and large and small mononuclear cell populations were analyzed by flow cytometry. Peripheral leukocyte population staining did not correlate with clinical signs or sensitization to PLP. Cryostat CNS tissue sections were stained with the same set of antibodies by using an immunoperoxidase technique, and positive cells and vessels were counted. T cells and macrophages were numerous and in equal numbers in perivascular parenchymal inflammatory infiltrates, whereas B cells were less numerous (p less than 0.001). T cells also diffusely infiltrated the parenchyma. Most perivascular inflammatory cells and many scattered parenchymal cells were Ia+; Ia vascular expression was increased over controls (p less than 0.001), and also correlated with disease severity. The immunopathology of this chronic EAE model is the same as that of whole CNS tissue- and myelin basic protein-induced EAE in other species, and is similar to that of multiple sclerosis. Cellular immune responses to PLP may therefore contribute to systemic and in situ responses in CNS tissue demyelinating diseases.
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PMID:The immunopathology of chronic experimental allergic encephalomyelitis induced in rabbits with bovine proteolipid protein. 241 15

A chronic form of experimental allergic encephalomyelitis can be produced by sensitization of rabbits with bovine myelin proteolipid apoprotein (PLP). To investigate the humoral immune response in this model, serum PLP antibodies were determined by enzyme-linked immunosorbent and dot immunobinding assays. In an initial experiment, 3 PLP-sensitized rabbits with severe chronic experimental allergic encephalomyelitis had a positive antibody response whereas 3 with mild disease, or with no visible clinical disease, had no detectable antibodies against PLP. In a second experiment, 3 rabbits were preimmunized with PLP in incomplete Freund's adjuvant, followed by a single immunization with PLP in complete Freund's adjuvant. These animals developed chronic experimental allergic encephalomyelitis with different progression rates, although all eventually became severely paralyzed. In both experiments the anti-PLP response was maximal before or immediately after disease onset and tended to decline during disease progression. The degree of the anti-PLP response correlated with clinical and histologic disease severity. These data suggest a possible role for humoral factors in the modulation of the chronic EAE induced in PLP-immunized rabbits.
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PMID:Chronic experimental allergic encephalomyelitis and antibody responses in rabbits immunized with bovine proteolipid apoprotein. 242 54

The suppressive effect of anti-L3T4 monoclonal antibody (mAb) on murine experimental allergic encephalomyelitis (EAE) induced by sensitization with proteolipid apoprotein (PLP) was examined in vivo and in vitro. This mAb inhibited the antigen-specific proliferation of the encephalitogenic T cell lines but did not block the mitogen-mediated response. Serial injections of the mAb during the pre-effector phase of EAE markedly suppressed the development and relapse of the disease but this treatment initiated after appearance of clinical signs was not effective. In treated animals, L3T4+ T cells in the spleen were profoundly decreased and the antigen-specific proliferative response of spleen cells was completely suppressed. Moreover, adoptive transfer of spleen cells from the treated mice induced resistance against EAE induction in the recipients. However, no obvious evidence for antigen-specific suppressor cells was found in vitro in the L3T4- populations of spleen cells from treated mice.
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PMID:In vivo and in vitro studies of the prevention of proteolipid apoprotein-induced murine experimental allergic encephalomyelitis by monoclonal antibody against L3T4. 245 81

Juvenile strain-13 guinea pigs challenged with whole central nervous system (CNS) tissue in complete Freund's adjuvant (CFA) developed chronic-relapsing (CR) experimental allergic encephalomyelitis (EAE). The animals that recovered from the first clinical episode were divided into three groups. One group was left untreated, one group was treated with three intracardiac injections of 100 micrograms glutaraldehyde-fixed myelin basic protein (MBP)-liposomes (MBP-L-GA) given once a week, and one group was treated with cytochrome c-liposomes (CYC-L-GA). The animals treated with MBP-liposomes were very well protected against further relapses. In vitro proliferative responses of peripheral blood lymphocytes (PBL) were performed repeatedly on most animals. The lymphocytes exhibited excellent proliferative responses to MBP, proteolipid apoprotein (PLP) and whole myelin, as well as to purified protein derivative (PPD) and concanavalin-A (ConA). High proliferative responses were recorded over the entire period of observation which lasted 12-22 months, each time the animals were tested in remission or in full relapse. However, a sharp decrease in proliferative responses was observed in most animals when the assay was performed 24-48 h before to 24 h after entering a relapse. The results demonstrate the presence of long-term and sustained cell-mediated responses to two distinct neuroantigens, and show fluctuations of both neuroantigen-specific and nonspecific responses concordant with a well-defined phase of the disease. Isoelectric focusing and immunofixation was performed on sera and cerebrospinal fluids obtained at the time of sacrifice. The pattern showed clear oligoclonal IgG bands (OB) in the samples obtained from untreated, CYC-L-GA-treated as well as in the MBP-L-GA-treated animals.
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PMID:Chronic-relapsing experimental allergic encephalomyelitis in strain-13 guinea pigs: cell-mediated immunity and IgG isoelectric focusing in myelin basic protein-liposome-treated and untreated animals. 246 97

Experimental allergic encephalomyelitis (EAE) is an autoimmune disease of the central nervous system (CNS). Its immune mechanism is well understood at the cellular and molecular levels, which is herein reviewed. Susceptibility to EAE is under the control of the genes partially inside and partially outside the H-2 complex. There are two myelin constituents known to be encephalitogenic, myelin basic protein and proteolipid apoprotein. EAE is mediated by effector T cells sensitized to the encephalitogen. Effector T cells bear surface phenotypes of Lyt1+2-, L3T4+, and they are activated by the encephalitogen/self Ia complex or certain alloantigens and acquire encephalitogenic activity. By unknown homing mechanisms, the effector T cells invade the CNS and induce the target phase phenomena, which include Ia-antigen expression in the local tissue, activation of procoagulant activity, breakdown of the blood-brain barrier, and excretion of lymphokines which induce inflammation and demyelination, resulting in functional alteration. Possibility of specific immune therapy is postulated as a model for human autoimmune disease.
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PMID:Cellular and molecular aspects of the pathomechanism and therapy of murine experimental allergic encephalomyelitis. 248 1

Experimental allergic encephalomyelitis (EAE) was induced in inbred Lewis rats by sensitization with bovine white matter proteolipid apoprotein (PLP). 18-61 days after a single injection of 100 micrograms of PLP, 12 of 31 rats (39%) developed clinical EAE and 18 of 23 (78%) showed pathologic EAE with significant demyelination. Lymphocyte proliferative responses and antibodies to PLP were elevated but did not correlate with the clinical or pathologic state. This is the first demonstration of PLP-induced EAE with significant demyelination in rats and will contribute to the study of autoimmune demyelination.
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PMID:Experimental allergic encephalomyelitis induced by proteolipid apoprotein in Lewis rats. 348 31

Experimental allergic encephalomyelitis (EAE) was successfully induced in BALB/c mice with DM-20, a protein component of proteolipid apoprotein. DM-20 was separated by ion exchange column chromatography with CM-Trisacryl from proteolipid apoprotein obtained from bovine spinal cords. Its purity was ascertained by SDS-polyacrylamide gel electrophoresis, a dot immunobinding procedure, and amino acid analysis. Nine of 15 animals with a single injection of 100 micrograms of DM-20 and five of seven animals with a booster injection developed hind leg paralysis or axial rotatory movement 16 to 27 days after sensitization (mean 21.3 days). Five of the 14 animals relapsed 2 to 6 wk after the first attack. Histological examination revealed inflammatory lesion, with significant demyelination in the central nervous system. Antibody levels to DM-20 were not related to the clinical signs. Five of 11 BALB/c nude mice reconstituted with T cells developed similar clinical and pathologic signs. This DM-20-induced EAE in mice may provide a valuable model because it is similar to multiple sclerosis and because it can be induced in inbred mice in which immune mechanisms can be easily studied.
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PMID:DM-20, a proteolipid apoprotein, is an encephalitogen of acute and relapsing autoimmune encephalomyelitis in mice. 349 Nov 50


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