Experimental allergic encephalomyelitis induced by the peptide encoded by exon 2 of the MBP gene, a peptide implicated in remyelination
Identifieur interne : 001295 ( Main/Exploration ); précédent : 001294; suivant : 001296Experimental allergic encephalomyelitis induced by the peptide encoded by exon 2 of the MBP gene, a peptide implicated in remyelination
Auteurs : Benjamin M. Segal [États-Unis] ; Cedric S. Raine [États-Unis] ; Dale E. Mcfarlin [États-Unis] ; Rhonda R. Voskuhl [États-Unis] ; Henry F. Mcfarland [États-Unis]Source :
- Journal of Neuroimmunology [ 0165-5728 ] ; 1994.
English descriptors
- Teeft :
- Adoptive, Adoptive transfer, Allergic encephalomyelitis, Amino acids, Antigenic, Antigenic challenge, Asymptomatic, Axon, Axonal dystrophy, Cell lines, Clinical grade, Clinical signs, Days post transfer, Demyelinated, Demyelinated axons, Demyelinating, Demyelination, Disease severity, Encephalitogenic, Encephalomyelitis, Entire neuroaxis, Epitope, Exon, Exon isoforms, Immunization, Immunodominant, Isoform, Isoforms, Lesion, Lncs, Lymphocyte, Mcfarland, Mcfarlin, Mouse, Multiple sclerosis, Murine, Myelin, Naive recipients, Neuroimmunology, Pathological analysis, Peptide, Point scale, Raine, Reae, Relapsing, Remyelination, Sclerosis, Segal, Spinal cord, Voskuhl.
Abstract
Abstract: The discovery of T lymphocytes reactive to the peptide encoded by exon 2 of the myelin basic protein (MBP) gene in multiple sclerosis (MS) patients has drawn attention to MBP isoforms harboring that peptide as candidate autoantigens. Previously, immunological studies in MS had almost exclusively used the more abundant 18.5 kDa isoform of MBP, which does not does not contain the exon 2 peptide. Investigations of experimental allergic encephalomyelitis (EAE) have also focussed on the 18.5 kDa MBP isoform and its peptides. Since EAE is an animal model widely used widly used to study MS, we examined the encephalitogenic potential of exon 2 peptide in the SJL/J mouse. Evidence for increased expression of exon 2-containing isoforms during remyelination in mouse CNS suggested that exon 2-sensitized T cels, with encephalitogenic capacity, might be important in the pertuation of relapsing EAE (rEAE). Our experiments have demonstrated that exon 2 peptide is inherently immunogenic in SJL mice and that EAE could be induced by the adoptive transfer of exon 2-sensitized lymphocytes. Furthermore, the disease could be accentuated by the transfer of short-term exon 2-reactive lines or by a combination of adoptive transfer and antigenic challenge with exon 2 peptide. The immunodominant epitope(s) appeared to localize to the segment bordered by amino acids 59–85.
Url:
DOI: 10.1016/0165-5728(94)90123-6
Affiliations:
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Mcfarlin</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Neuroimmunology Branch, NINDS, Building 10, Room 5B16, NIH, Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Voskuhl, Rhonda R" sort="Voskuhl, Rhonda R" uniqKey="Voskuhl R" first="Rhonda R." last="Voskuhl">Rhonda R. Voskuhl</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Neuroimmunology Branch, NINDS, Building 10, Room 5B16, NIH, Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Mcfarland, Henry F" sort="Mcfarland, Henry F" uniqKey="Mcfarland H" first="Henry F." last="Mcfarland">Henry F. Mcfarland</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Neuroimmunology Branch, NINDS, Building 10, Room 5B16, NIH, Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neuroimmunology</title><title level="j" type="abbrev">JNI</title><idno type="ISSN">0165-5728</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1994">1994</date><biblScope unit="volume">51</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="7">7</biblScope><biblScope unit="page" to="19">19</biblScope></imprint><idno type="ISSN">0165-5728</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0165-5728</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Adoptive</term><term>Adoptive transfer</term><term>Allergic encephalomyelitis</term><term>Amino acids</term><term>Antigenic</term><term>Antigenic challenge</term><term>Asymptomatic</term><term>Axon</term><term>Axonal dystrophy</term><term>Cell lines</term><term>Clinical grade</term><term>Clinical signs</term><term>Days post transfer</term><term>Demyelinated</term><term>Demyelinated axons</term><term>Demyelinating</term><term>Demyelination</term><term>Disease severity</term><term>Encephalitogenic</term><term>Encephalomyelitis</term><term>Entire neuroaxis</term><term>Epitope</term><term>Exon</term><term>Exon isoforms</term><term>Immunization</term><term>Immunodominant</term><term>Isoform</term><term>Isoforms</term><term>Lesion</term><term>Lncs</term><term>Lymphocyte</term><term>Mcfarland</term><term>Mcfarlin</term><term>Mouse</term><term>Multiple sclerosis</term><term>Murine</term><term>Myelin</term><term>Naive recipients</term><term>Neuroimmunology</term><term>Pathological analysis</term><term>Peptide</term><term>Point scale</term><term>Raine</term><term>Reae</term><term>Relapsing</term><term>Remyelination</term><term>Sclerosis</term><term>Segal</term><term>Spinal cord</term><term>Voskuhl</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The discovery of T lymphocytes reactive to the peptide encoded by exon 2 of the myelin basic protein (MBP) gene in multiple sclerosis (MS) patients has drawn attention to MBP isoforms harboring that peptide as candidate autoantigens. Previously, immunological studies in MS had almost exclusively used the more abundant 18.5 kDa isoform of MBP, which does not does not contain the exon 2 peptide. Investigations of experimental allergic encephalomyelitis (EAE) have also focussed on the 18.5 kDa MBP isoform and its peptides. Since EAE is an animal model widely used widly used to study MS, we examined the encephalitogenic potential of exon 2 peptide in the SJL/J mouse. Evidence for increased expression of exon 2-containing isoforms during remyelination in mouse CNS suggested that exon 2-sensitized T cels, with encephalitogenic capacity, might be important in the pertuation of relapsing EAE (rEAE). Our experiments have demonstrated that exon 2 peptide is inherently immunogenic in SJL mice and that EAE could be induced by the adoptive transfer of exon 2-sensitized lymphocytes. Furthermore, the disease could be accentuated by the transfer of short-term exon 2-reactive lines or by a combination of adoptive transfer and antigenic challenge with exon 2 peptide. The immunodominant epitope(s) appeared to localize to the segment bordered by amino acids 59–85.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="Maryland"><name sortKey="Segal, Benjamin M" sort="Segal, Benjamin M" uniqKey="Segal B" first="Benjamin M." last="Segal">Benjamin M. Segal</name></region><name sortKey="Mcfarland, Henry F" sort="Mcfarland, Henry F" uniqKey="Mcfarland H" first="Henry F." last="Mcfarland">Henry F. Mcfarland</name><name sortKey="Mcfarlin, Dale E" sort="Mcfarlin, Dale E" uniqKey="Mcfarlin D" first="Dale E." last="Mcfarlin">Dale E. Mcfarlin</name><name sortKey="Raine, Cedric S" sort="Raine, Cedric S" uniqKey="Raine C" first="Cedric S." last="Raine">Cedric S. Raine</name><name sortKey="Voskuhl, Rhonda R" sort="Voskuhl, Rhonda R" uniqKey="Voskuhl R" first="Rhonda R." last="Voskuhl">Rhonda R. Voskuhl</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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