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)

Discrete populations of anti-S49 antibodies were found in the antisera of Lewis rats recovered from S49-induced experimental allergic encephalomyelitis (EAE). A potent inducer of EAE in Lewis rats, S49 is a synthetic peptide representing residues 69-84 of bovine myelin basic protein but with deletions at Gly-77 and His-78 to form an analogue of guinea pig or rat 69-84, GSLPQKAQRPQDENG. Each population within a given antiserum, as identified by Scatchard and Sipsian window analysis, was found to exhibit reactivity for a different S49 determinant, and the affinities of each population were relatively restricted and discontinuous. The high affinity populations (10(7)-10(8) M-1) were cross-reactive with YS8 (YGSLPQKAQGHRPQDENG) in equilibrium competitive inhibition reactions whereas the low affinity populations (10(5)-10(6) M-1) were reactive only with S49 and YS49 among a panel of peptide analogues. Of the YS8 cross-reactive antibodies the highest affinity (10(8) M-1) were also cross reactive with S81 (YGSLPQKAQGHRPQDEG) but not S49 (69-84-Gly), thus emphasizing the need for Tyr-68 for format stability of the determinant involved. The other YS8 cross-reactive population (10(7) M-1) was completely reactive with S49 but totally unreactive with S81 in equilibrium reactions, thus emphasizing the requirement for Asn-84 but not Tyr-68 for the determinant's topographic stability. Peptides shorter than S49 from the N-terminal end, but retaining the sequences AQRPQDEN or SQRSQDEN (suspected residence of minimal encephalitogenic determinants), reacted only under conditions of two-step non-equilibrium competitive inhibition assays. Such reactions would occur only at very low affinity (less than 10(5) M-1) with the anti-S49 antibodies. It was hypothesized that the encephalitogenic T-cell determinant for Lewis rats, although permitting B-cell responses at very low affinity, may exclude high affinity responses in susceptible animals.
Neurochem Res 1985 Dec
PMID:Immunochemical analysis of Lewis rat antisera to the synthetic encephalitogenic peptide S49. 241 80

We studied the ability of alpha-fetoprotein (AFP) to suppress experimental allergic encephalomyelitis (EAE) in rabbits. Animals were treated with daily injections of 50 micrograms of AFP following the onset of neurological signs. Clinical status, anti-myelin basic protein (MBP) antibody titers, and histopathological changes in the CNS were determined. Treatment with AFP significantly improved the clinical scores of the affected rabbits and inhibited the binding of anti-MBP antibodies to MBP in vitro. However, there was no significant difference in the titers of anti-MBP antibody, and no amelioration of histopathological changes between treated and control animals. We conclude that AFP is effective in improving the clinical status of animals with EAE, even after the appearance of clinical signs.
Isr J Med Sci 1985 Dec
PMID:Treatment of experimental allergic encephalomyelitis in rabbits with alpha-fetoprotein. 241 77

Lymph node cells from SJL mice immunized with guinea pig myelin basic protein proliferate in vitro to the same antigen. This proliferative response is abolished by depletion of macrophages-monocytes, but can be reconstituted by the addition of cerebral vascular endothelial cells (EC) freshly isolated from syngeneic mice with adoptively transferred acute experimental allergic encephalomyelitis (EAE). Reconstitution by EC from mice with EAE can be blocked by pretreatment of EC with syngeneic anti-I-A antisera. Freshly isolated EC from normal syngeneic mice do not restore responsiveness, but can be induced to present antigen by culture with murine recombinant immune interferon-gamma or supernatants from a variety of immune cell cultures. These findings are consistent with the hypothesis that immune cells release interferon and/or other soluble factors which induce I-A molecules on EC, which subsequently acquire the capacity to present antigen. The implications of these findings relate to the migration of cells across the blood-brain-barrier into the central nervous system, and are of importance in the understanding of the pathogenesis of several neurologic disorders.
J Immunol 1986 Dec 01
PMID:Interaction between myelin basic protein-sensitized T lymphocytes and murine cerebral vascular endothelial cells. 243 Oct 34

Rabies vaccine produced in rhesus diploid cells (RDRV) and adsorbed on aluminium phosphate was evaluated for its neurological safety in guinea pigs and Lewis rats. The vaccine (as well as aluminium phosphate itself) in combination with myelin basic protein did not induce experimental allergic encephalomyelitis (EAE) when injected into either species. RDRV combined with complete Freund's adjuvant still failed to induce any signs of EAE. In contrast, basic protein combined with complete Freund's adjuvant induced severe EAE in both guinea pigs and rats. No experimental evidence was obtained to indicate adverse neuroimmunological activity of RDRV.
Vaccine 1986 Dec
PMID:Rhesus diploid rabies vaccine (adsorbed): neurological safety in guinea pigs and Lewis rats. 243 37

Experimental autoimmune encephalomyelitis (EAE) and/or tuberculin sensitivity were transferred to histocompatible recipients with myelin basic protein-stimulated and/or PPD stimulated guinea pig lymph node T cells previously separated by depletion of B cells ("panning") on rabbit anti-guinea pig Ig antibody-coated Petri plates. The depletion was augmented by complement-mediated lysis using mouse anti-guinea pig B-cell monoclonal antibody (31D2), rabbit anti-mouse Ig, and rabbit complement. B cells did not transfer EAE nor provide protection against active immunization with guinea pig spinal cord antigen.
Cell Immunol 1986 Dec
PMID:Transfer of autoimmune encephalomyelitis with T lymphocytes in strain 13 guinea pigs. 243 54

Highly purified rat fibroblast-derived interferon (RfIFN), was administered intraventricularly to Lewis rats affected with experimental autoimmune encephalomyelitis (EAE). Its effects on both the active and passive forms of EAE were studied. A method was devised to deliver, via a syringe pump, RfIFN (sp. act. 10(8) U/mg) into the third ventricle of control and experimental animals. Rats with either the active form of EAE (produced by injection with myelin basic protein (MBP) in Freund's complete adjuvant) or with adoptively transferred EAE were treated with RfIFN either therapeutically and/or prophylactically. In no instance was a significant difference observed, on the course of EAE, between those animals receiving RfIFN and those receiving "mock" IFN. The pharmacokinetics of the infused RfIFN were also studied.
J Interferon Res 1986 Dec
PMID:Interferon in experimental autoimmune encephalomyelitis: intraventricular administration. 243 23

The in vivo administration of monoclonal antibody (mAb) to the CD4 antigen associated with helper T cells has been successful in prolonging the survival of nonhuman primates with experimental allergic encephalomyelitis (EAE). EAE was induced in 17 outbred longtailed macaques (Macaca fascicularis) by inoculation of homologous myelin basic protein (BP) in complete Freund's adjuvant (CFA). Treatment was begun at the onset of clinical signs. Eleven animals were treated with anti-CD4 mAb Leu3a (eight) or OKT4a (three). Of the six control animals, two received anti-CD8 mAb (Leu2a), and four were treated with saline. Specific T- and B-cell subsets which have been implicated in the development of EAE were monitored throughout the course of the disease by one- and two-color immunofluorescence (IF). The monkey anti-BP antibody and anti-mouse immunoglobulin (IgG) responses were measured by enzyme-linked immunoassay (ELISA) techniques, as were the levels of free-circulating murine IgG. The nature of the infiltrating lymphocytes in the brain was evaluated histologically post mortem. Our results indicate that anti-CD4 mAb can prolong survival and in some cases completely reverse the clinical appearance of the disease; however, relapses did occur. Treatments with Leu3a or OKT4a anti-CD4 mAbs reversed the ongoing depletion of CD4+ and CD8+ cells caused by the development of EAE and appeared to reduce the size and degree of inflammation in brain lesions. These treatments did not induce immunologic tolerance to mouse IgG since all of the anti-CD4-treated animals produced high titers of anti-mouse IgG antibodies. Treatment with Leu2a (anti-CD8) had no effect on the development of EAE. These results suggest that CD4+ cells are important to the pathogenesis of EAE in macaques and that manipulation of this subset with monoclonal antibodies may provide effective treatment of human demyelinating disease.
Clin Immunol Immunopathol 1987 Dec
PMID:In vivo administration of anti-CD4 monoclonal antibody prolongs survival in longtailed macaques with experimental allergic encephalomyelitis. 244 10

Antigen targeting of liposome-encapsulated cytotoxic drugs to specific lymphocytes may be a useful approach for antigen-specific immunosuppressive treatment of autoimmune diseases in which a specific antigen is involved. The feasibility of utilizing this approach was investigated using experimental allergic encephalomyelitis as an animal model for an autoimmune response. The encephalitogenic determinant of myelin basic protein for the guinea pig is contained in residues 114-122, the so-called nonapeptide. We have acylated the nonapeptide at its N-terminal to anchor it in the lipid bilayer of liposomes containing the cytotoxic drug methotrexate. The nonapeptide on the surface of the liposomes then allows targeting of the liposomal methotrexate in vitro to anti-nonapeptide T lymphocytes obtained from guinea pigs with experimental allergic encephalomyelitis. Treatment with the nonapeptide-targeted liposomal methotrexate inhibited proliferation of anti-nonapeptide lymphocytes significantly more than that of control lymphocytes. These included non-sensitized lymphocytes, stimulated with phytohemagglutinin, or lymphocytes sensitized to different, unrelated proteins, the purified protein derivative of tuberculin and keyhole limpet hemocyanin, and stimulated with their specific antigens. Furthermore, nonapeptide-targeted liposomes had a greater cytotoxic effect on anti-nonapeptide T cells than untargeted liposomes. The results indicated that specific targeting to and killing of anti-nonapeptide cells was achieved, although improvements of the treatment are necessary before its use can be attempted in vivo.
J Neuroimmunol 1987 Dec
PMID:Antigen-targeted liposome-encapsulated methotrexate specifically kills lymphocytes sensitized to the nonapeptide of myelin basic protein. 244 75

Antibody responses to the myelin/oligodendrocyte glycoprotein (MOG) and myelin basic protein (MBP) were determined in the sera of Hartley guinea pigs with chronic relapsing experimental allergic encephalomyelitis (CREAE) using an enzyme-linked immunoassay. The sera were also tested for in vivo demyelinating activity by infusion into the subarachnoid space of normal rats. In contrast to the MBP titres, the anti-MOG antibody titres showed good correlation with the in vivo demyelinating activity of the sera (r = 0.91, P less than 0.001). This result suggests that antibodies directed against MOG may be involved in the pathogenesis of demyelination in CREAE.
J Neuroimmunol 1987 Dec
PMID:Antibody responses in chronic relapsing experimental allergic encephalomyelitis: correlation of serum demyelinating activity with antibody titre to the myelin/oligodendrocyte glycoprotein (MOG). 244 77

Experimental allergic orchitis (EAO) and experimental allergic encephalomyelitis (EAE) are animal models of organ-specific autoimmune disease. In this study, BALB/cByJ and BALB/cAnNCr mice were susceptible to both autoimmune diseases whereas BALB/cJ subline mice were resistant. Disease resistance in BALB/cJ mice did not appear to be a reflection of either (i) a nonspecific generalized impairment of cellular immunity or (ii) an alteration in the phenotypic expression of Bordetella pertussis-induced histamine sensitization, a phenotype which has been shown to be associated with susceptibility to both diseases. Susceptibility to both EAE and EAO was inherited as a dominant trait in F1 hybrid animals. Segregation analysis in a (BALB/cByJ X BALB/cJ) X BALB/cJ backcross population suggested that disease resistance may be associated with a single genotypic difference in a common regulatory gene affecting susceptibility to both diseases. Linkage analysis of the backcross population failed to demonstrate an association of disease resistance with the mutant raf-1b allele carried by BALB/cJ mice. The results of these studies support previous observations that multiple genotypic differences may in fact exist in mice of the BALB/cJ subline and that such differences play a significant role in the genetic control of susceptibility to EAE and EAO.
Cell Immunol 1987 Dec
PMID:Differential susceptibility to actively induced experimental allergic encephalomyelitis and experimental allergic orchitis among BALB/c substrains. 244 78


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