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)

To clarify the functional role of the I region-associated (Ia) antigen in autoimmune central nervous system disorders, we generated long-term cultured lines of encephalitogenic T cells responsive to myelin basic protein from SJL strain mice (H-2s) and investigated genetic restriction in proliferative and encephalitogenic activities of the lines. These cell lines bear a Lyt 1+,2- phenotype, and show antigen-specific and I-As restricted proliferative responses in vitro. These lines induced full-blown experimental allergic encephalomyelitis (EAE) in immuno-compromised recipients carrying the I-As genotype. These data demonstrate that encephalitogenic T lymphocytes recognize the antigen in combination with the Ia antigen to induce EAE.
J Neuroimmunol 1985 Sep
PMID:Ia restriction of murine encephalitogenic T-cell lines in vitro and in vivo. 241 Apr 53

Mononuclear cells extracted from regional lymph nodes, blood, spleen and central nervous system of guinea pigs with chronic relapsing experimental allergic encephalomyelitis (r-EAE), adjuvant immunized and untreated controls were cultured for 16 h in microtitre plates, and culture supernatants were then used to measure IgG and IgM, as well as IgG class anti-myelin antibody production by enzyme-linked immunosorbent assays. Increased synthesis of these immunoglobulins and antibodies was found during the course of r-EAE both in intra- and extrathecal compartments. Long-term cultures carried out for 7 days gave similar results but anti-myelin, anti-myelin basic protein and IgG synthesis was most pronounced intrathecally. Agarose isoelectric focusing of supernatants from these cultures showed oligoclonal IgG. These findings indicate in vivo synthesis of autoantibodies within the target for immune attack and a partial sequestration of the immune response to this compartment.
J Neuroimmunol 1985 Sep
PMID:In vitro synthesis of immunoglobulins and autoantibodies by lymphocytes from various body compartments during chronic relapsing experimental allergic encephalomyelitis. 241 Apr 54

The loss of myelin-associated glycoprotein (MAG) and myelin basic protein (MBP) was compared by quantitative immunocytochemistry in demyelinating lesions of measles encephalomyelitis (ME), multiple sclerosis (MS), and progressive multifocal leukoencephalopathy (PML). Serial sections from paraffin-embedded tissue were reacted with antisera for MAG and MBP, and areas of staining loss were compared morphometrically. Lesions in ME showed MAG loss equal to that of MBP, lesions of PML showed MAG loss greater than that of MBP, and MS lesions showed a mixture of patterns. These data demonstrate distinctive patterns of MAG and MBP loss in these three diseases.
Ann Neurol 1985 Sep
PMID:A quantitation of myelin-associated glycoprotein and myelin basic protein loss in different demyelinating diseases. 241 98

The pathology of experimental allergic encephalomyelitis (EAE) induced by bovine myelin basic protein (MBP) has been examined in the guinea pig with a series of doses ranging from 37.5 micrograms to 600 micrograms. This was to investigate whether the previously demonstrated lack of demyelinative effect by MBP was dose-related. At all doses tested, MBP induced clinical disease. Inflammation was the major feature of lesions in all animals. However, no demyelination was seen when 75 micrograms MBP or less was given. At higher doses (150 micrograms upwards), MBP always induced intense inflammation but demyelination was encountered inconsistently. These observations support the contention that in addition to an immune response to MBP, other factors contribute to autoimmune demyelination.
J Neurol Sci 1985 Sep
PMID:Dose-dependency of MBP-induced demyelination in the guinea pig. 241 4

Experimental allergic encephalomyelitis could be induced in rabbits by injection in Freund's complete adjuvant of either peptide 1-44 or peptide 45-87 of rabbit myelin basic protein. In order to localize the encephalitogenic determinant present in peptide 1-44, several smaller derivative peptides were prepared and examined. Peptic peptide 15-44 and thrombic peptide 1-31 were as active as peptide 1-44, whereas peptic peptides 1-14 and 18-38 and BrCN peptide 22-44 were virtually inactive. Weak activity was shown by BrCN peptide 1-21. These results provide evidence that a major encephalitogenic determinant present in peptide 1-44 lies within sequence 15-31. The encephalitogenic activity of peptide 15-44 was essentially destroyed by oxidation of methionine-21 to methionine sulfoxide; methylation of Met-21, on the other hand, appeared to be relatively ineffective in eliminating the encephalitogenicity of peptide 1-44.
J Neuroimmunol 1986 Sep
PMID:Experimental allergic encephalomyelitis in rabbits. A major encephalitogenic determinant within residues 1-44 of myelin basic protein. 242 3

Experimental allergic encephalomyelitis (EAE) is an animal model of T cell-mediated, central nervous system neuropathology that may be a relevant animal model for multiple sclerosis. EAE is usually induced by sensitization of animals with a xenogeneic myelin basic protein (MBP). Recently, MBP-reactive T cell lines and clones derived from lymphoid tissue of animals with EAE have proved very useful in elucidating certain aspects of the pathogenesis in EAE. However, questions relating to how T cells actually mediate the pathologic changes seen in EAE remain unresolved. We now report for the first time the derivation of long-term, interleukin 2-dependent T cell lines and sublines from a site of pathology in murine EAE--the spinal cord. All of the spinal cord-derived T cell lines and sublines were found to be "autoreactive" in that they responded to self (murine) MBP as well as to the xenogeneic immunogen, porcine MBP. The ability to derive T cell lines and sublines from the spinal cords of mice with EAE should now aid in the elucidation of pathogenetic mechanisms in EAE by allowing for a characterization of those T cells found at the site of pathology.
J Immunol 1986 Sep 15
PMID:T cell lines derived from the spinal cords of mice with experimental allergic encephalomyelitis are self reactive. 242 82

Immunization with myelin basic protein (BP) causes experimental allergic encephalomyelitis (EAE) in certain strains of mice. SJL/J (H-2s) is the prototype sensitive strain. Although BALB/c (H-2d) is resistant to EAE through use of an identical immunization protocol, (BALB/c x SJL/J)F1 hybrid mice develop EAE after immunization with BP. T cell clones specific for BP have been isolated from a highly encephalitogenic line of (BALB/c x SJL/J)F1 hybrid T cells raised against bovine BP. The clones were examined for their H-2 restriction and specificity for heterologous forms of BP (mouse, rat, and bovine BP). The results revealed the clones cross-reacting with mouse (self) BP were almost always restricted to F1 hybrid class II major histocompatibility complex (MHC) elements. In contrast, mouse cross-reactive clones derived from a nonencephalitogenic (BALB/c x SJL/J) T cell line raised against rat BP were largely restricted to H-2d elements. These clones did not cross-react with bovine BP. Four additional lines were generated by carrying the original rat and bovine F1 T cell lines on parental antigen-presenting cells thus generating lines biased toward homozygous (SJL/J, H-2s, or BALB/c, H-2d) restriction elements. These "parentally restricted" T cell lines did not induce EAE when injected in vivo. These results suggest that in this F1 strain sensitivity to T cell-induced EAE is associated with epitopes on murine BP that associate with F1 class II MHC restricting elements. In contrast, nonencephalitogenic T cell lines contain a high proportion of murine cross-reactive clones restricted to H-2d, the haplotype of the classically resistant BALB/c mouse. This work illustrates the use of T cell lines and clones in a model system to further analyze the role of MHC restriction elements in autoimmune disease occurring in heterozygous individuals.
J Immunol 1987 Sep 15
PMID:Comparison of antigen specificity, class II major histocompatibility complex restriction, and in vivo behavior of myelin basic protein-specific T cell lines and clones derived from (BALB/c x SJL/J) mice. 244 57

Adherence of red blood cells from SJL mice suffering of chronic relapsing experimental allergic encephalomyelitis was studied to myelin basic protein coated microtiter plates. Control animals received either bovine serum albumine or "protein-antigen free" adjuvant using the same immunization protocol. Characteristic changes in adherence were found in bovine or human myelin basic protein injected animals compared to the bovine serum albumine immunized group. After a nonspecific increase in adherence between Days 2 to 6 observed in all 3 groups, in the encephalitogen challenged animals on Days 13-14 a marked decrease in red blood cell adherence was detected which maintained at this decreased level during the clinically active stage of the disease and reappeared with the relapse of EAE. No such decreased adherence of red blood cells was observed in BSA immunized animals or in adherence of cells from myelin basic protein injected animals to other basic type protein such as histone. Thus, decreased adherence of red blood cells in animals with EAE appears to be an interestingly unique measure of the disease activity.
Acta Neurol Scand 1987 Sep
PMID:Adherence of cells to myelin basic protein. II. Adherence of red blood cells of SJL mice with chronic relapsing EAE. 244 62

We generated Theiler's murine encephalomyelitis virus mutants resistant to several neutralizing monoclonal antibodies (MAbs) having their epitopes near a trypsin cleavage site of VP1. Neutralization and Western blot (immunoblot) studies suggest that two of the MAbs have identical epitopes that partly overlap the epitope of a third MAb. Sequencing of RNA of the mutants localized the epitopes to a site near the carboxyl end of VP1. The limited diversity of nucleotide changes seen in the mutants and the immunodominance of the site suggest that the carboxyl end of VP1 may have an important function.
J Virol 1988 Sep
PMID:Trypsin-sensitive neutralization site on VP1 of Theiler's murine encephalomyelitis viruses. 245 18

Experimental allergic encephalomyelitis (EAE)-susceptible Lew and EAE-resistant Brown Norway (BN) rats and the corresponding MHC congenic strains were examined for their ability to develop clinical and histologic EAE. The ability of T cells from these animals to proliferate in vitro in response to whole guinea pig (GP) myelin basic protein (MBP), rat MBP, and to the major encephalitogenic peptide of GP MBP 66-88 (GP 68-88) was also assessed. We found that Lewis (Lew) was highly susceptible and showed good T cell responses to GP, MBP, rat MBP, and GP 68-88. Lew.1N (BN MHC on Lew background) and BN were not susceptible and T cells from these strains showed significant responses to GP MBP, but not to rat MBP or GP 68-88. Although BN.B1 (Lew MHC on BN background) was not susceptible to actively induced EAE, MBP-specific Lew T cells could transfer severe disease to BN.B1. BN.B1 T cells showed responses to GP-MBP, rat MBP, and GP 68-88 and, when transferred to naive BN.B1 or Lew, induced only mild clinical EAE in both strains. Increasing the number of T cells from BN.B1 had no effect on the severity of clinical symptoms in either recipient, suggesting some deficiency in the T cell repertoire that is necessary for induction of severe EAE. These results suggest that 1) the T cell response to rat MBP and GP68-88 (but not to sites other than 68-88 in GP MBP) is necessary for susceptibility to EAE; 2) the ability to respond to both rat MBP and GP 68-88 is determined by the MHC gene products on APC; and 3) given a permissive MHC, the T cell response that results in EAE is influenced by non-MHC genes.
J Immunol 1988 Sep 01
PMID:Genetic control of the development of experimental allergic encephalomyelitis in rats. Separation of MHC and non-MHC gene effects. 245 18


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