Impaired late suppression of Epstein-Barr virus (EBV)-induced immunoglobulin synthesis: A common feature of autoimmune disease
Identifieur interne : 003170 ( Main/Exploration ); précédent : 003169; suivant : 003171Impaired late suppression of Epstein-Barr virus (EBV)-induced immunoglobulin synthesis: A common feature of autoimmune disease
Auteurs : A. Shore [Canada] ; Rhonda Klock [Canada] ; P. Lee [Canada] ; Krista M. Snow [Canada] ; E. C. Keystone [Canada]Source :
- Journal of Clinical Immunology [ 0271-9142 ] ; 1989-03-01.
English descriptors
- KwdEn :
- Teeft :
- Active articular disease, Arth rheum, Arthritis, Assay, Autoimmune, Autoimmune disease, Clinical immunology, Common feature, Cystic fibrosis, Defect, Defective regulation, Diagnostic criteria, Disease activity, Drug therapy, Ebv, Ebvs titer, High titers, Immunology, Late suppression, Lymphocyte, Lymphocyte subsets, Normal controls, Normal regulation, Patient groups, Peak proliferation, Peak proliferative response, Peak response, Percentage suppression, Peripheral blood, Proliferation, Proliferative, Proliferative response, Regulatory defect, Rheumatoid, Rheumatoid arthritis, Sequential time kinetics, Seronegative arthritis, Seronegative arthropathies, Suppression, Systemic lupus erythematosus, Time kinetics, Wellesley hospital.
Abstract
Abstract: We examined regulation of Epstein-Barr virus-induced plaque-forming cell generation in peripheral blood mononuclear cells from several autoimmune and seronegative diseases and correlated these results with Epstein-Barr virus-induced proliferation. We confirmed the defective regulation of Epstein-Barr virus-induced plaque-forming cells in peripheral blood mononuclear cells of patients with rheumatoid arthritis and scleroderma. Peripheral blood mononuclear cells from patients with seronegative arthropathies and chronic infective inflammation (cystic fibrosis) had normal regulation of Epstein-Barr virus-induced plaque-forming cells. Peripheral blood mononuclear cells from rheumatoid arthritis had excessive plaque-forming cell generation in the face of a normally regulated decrease in Epstein-Barr virus-induced proliferation. In contrast, peripheral blood mononuclear cells from scleroderma had defective suppression of both Epstein-Barr virus-induced proliferation and plaque-forming cell generation. Thus, impaired regulation of Epstein-Barr virus-induced plaque-forming cell generation is a common feature of autoimmune disease and demonstrates some specificity for these disorders.
Url:
DOI: 10.1007/BF00916937
Affiliations:
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Shore</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Medicine, Rheumatic Disease Unit Research Laboratories, The Wellesley Hospital and The Research Institute, Hospital for Sick Children, Toronto</wicri:regionArea><wicri:noRegion>Toronto</wicri:noRegion></affiliation></author><author><name sortKey="Klock, Rhonda" sort="Klock, Rhonda" uniqKey="Klock R" first="Rhonda" last="Klock">Rhonda Klock</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Medicine, Rheumatic Disease Unit Research Laboratories, The Wellesley Hospital and The Research Institute, Hospital for Sick Children, Toronto</wicri:regionArea><wicri:noRegion>Toronto</wicri:noRegion></affiliation></author><author><name sortKey="Lee, P" sort="Lee, P" uniqKey="Lee P" first="P." last="Lee">P. Lee</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Medicine, Rheumatic Disease Unit Research Laboratories, The Wellesley Hospital and The Research Institute, Hospital for Sick Children, Toronto</wicri:regionArea><wicri:noRegion>Toronto</wicri:noRegion></affiliation></author><author><name sortKey="Snow, Krista M" sort="Snow, Krista M" uniqKey="Snow K" first="Krista M." last="Snow">Krista M. Snow</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Medicine, Rheumatic Disease Unit Research Laboratories, The Wellesley Hospital and The Research Institute, Hospital for Sick Children, Toronto</wicri:regionArea><wicri:noRegion>Toronto</wicri:noRegion></affiliation></author><author><name sortKey="Keystone, E C" sort="Keystone, E C" uniqKey="Keystone E" first="E. C." last="Keystone">E. C. Keystone</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Medicine, Rheumatic Disease Unit Research Laboratories, The Wellesley Hospital and The Research Institute, Hospital for Sick Children, Toronto</wicri:regionArea><wicri:noRegion>Toronto</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Clinical Immunology</title><title level="j" type="abbrev">J Clin Immunol</title><idno type="ISSN">0271-9142</idno><idno type="eISSN">1573-2592</idno><imprint><publisher>Kluwer Academic Publishers-Plenum Publishers</publisher><pubPlace>New York</pubPlace><date type="published" when="1989-03-01">1989-03-01</date><biblScope unit="volume">9</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="103">103</biblScope><biblScope unit="page" to="110">110</biblScope></imprint><idno type="ISSN">0271-9142</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0271-9142</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Epstein-Barr virus (EBV)</term><term>T cell</term><term>immunoregulation</term><term>rheumatoid arthritis</term><term>scleroderma</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Active articular disease</term><term>Arth rheum</term><term>Arthritis</term><term>Assay</term><term>Autoimmune</term><term>Autoimmune disease</term><term>Clinical immunology</term><term>Common feature</term><term>Cystic fibrosis</term><term>Defect</term><term>Defective regulation</term><term>Diagnostic criteria</term><term>Disease activity</term><term>Drug therapy</term><term>Ebv</term><term>Ebvs titer</term><term>High titers</term><term>Immunology</term><term>Late suppression</term><term>Lymphocyte</term><term>Lymphocyte subsets</term><term>Normal controls</term><term>Normal regulation</term><term>Patient groups</term><term>Peak proliferation</term><term>Peak proliferative response</term><term>Peak response</term><term>Percentage suppression</term><term>Peripheral blood</term><term>Proliferation</term><term>Proliferative</term><term>Proliferative response</term><term>Regulatory defect</term><term>Rheumatoid</term><term>Rheumatoid arthritis</term><term>Sequential time kinetics</term><term>Seronegative arthritis</term><term>Seronegative arthropathies</term><term>Suppression</term><term>Systemic lupus erythematosus</term><term>Time kinetics</term><term>Wellesley hospital</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: We examined regulation of Epstein-Barr virus-induced plaque-forming cell generation in peripheral blood mononuclear cells from several autoimmune and seronegative diseases and correlated these results with Epstein-Barr virus-induced proliferation. We confirmed the defective regulation of Epstein-Barr virus-induced plaque-forming cells in peripheral blood mononuclear cells of patients with rheumatoid arthritis and scleroderma. Peripheral blood mononuclear cells from patients with seronegative arthropathies and chronic infective inflammation (cystic fibrosis) had normal regulation of Epstein-Barr virus-induced plaque-forming cells. Peripheral blood mononuclear cells from rheumatoid arthritis had excessive plaque-forming cell generation in the face of a normally regulated decrease in Epstein-Barr virus-induced proliferation. In contrast, peripheral blood mononuclear cells from scleroderma had defective suppression of both Epstein-Barr virus-induced proliferation and plaque-forming cell generation. Thus, impaired regulation of Epstein-Barr virus-induced plaque-forming cell generation is a common feature of autoimmune disease and demonstrates some specificity for these disorders.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Shore, A" sort="Shore, A" uniqKey="Shore A" first="A." last="Shore">A. Shore</name></noRegion><name sortKey="Keystone, E C" sort="Keystone, E C" uniqKey="Keystone E" first="E. C." last="Keystone">E. C. Keystone</name><name sortKey="Klock, Rhonda" sort="Klock, Rhonda" uniqKey="Klock R" first="Rhonda" last="Klock">Rhonda Klock</name><name sortKey="Lee, P" sort="Lee, P" uniqKey="Lee P" first="P." last="Lee">P. Lee</name><name sortKey="Snow, Krista M" sort="Snow, Krista M" uniqKey="Snow K" first="Krista M." last="Snow">Krista M. Snow</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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