Defective production of interleukin-2 in patients with idiopathic Parkinson's disease
Identifieur interne : 003106 ( Main/Corpus ); précédent : 003105; suivant : 003107Defective production of interleukin-2 in patients with idiopathic Parkinson's disease
Auteurs : Harald Klüter ; Peter Vieregge ; Henning Stolze ; Holger KirchnerSource :
- Journal of the Neurological Sciences [ 0022-510X ] ; 1995.
Abstract
The pathogenesis of Parkinson's disease (PD) is largely unknown. Recently, several studies have presented evidence of an immunological dysfunction in patients suffering from PD. We studied the immune responsiveness of patients with idiopathic PD (n = 20) by investigation of the ability of peripheral blood mononuclear cells to produce cytokines after mitogenic stimulation in a whole blood assay. A group of age-related healthy blood donors served as control (n = 19). Additionally, white blood count, leukocyte differentiation and lymphocyte subtyping were performed. PD patients had a significantly higher neutrophil count, but analysis of T-cell subsets showed no difference between the two groups. In peripheral blood, secretion of interleukin-2 (IL-2) after mitogenic stimulation was significantly diminished in the patients' group (p < 0.01), whereas values of IFN-α2, IL-6, IFN-γ and sIL-2R were comparable in both groups. IL-2 production correlated negatively with the mean annual dose of levodopa treatment and correlated significantly (p < 0.002) with amantadine uptake. Analysis of sex, age, duration of illness and other drug intake revealed no correlation with cytokine release. Our findings support the view that there is a selective abnormality in the immune repertoire of peripheral blood lymphocytes in patients suffering from PD, the reasons for which need to be explored.
Url:
DOI: 10.1016/0022-510X(95)00180-A
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Recently, several studies have presented evidence of an immunological dysfunction in patients suffering from PD. We studied the immune responsiveness of patients with idiopathic PD (n = 20) by investigation of the ability of peripheral blood mononuclear cells to produce cytokines after mitogenic stimulation in a whole blood assay. A group of age-related healthy blood donors served as control (n = 19). Additionally, white blood count, leukocyte differentiation and lymphocyte subtyping were performed. PD patients had a significantly higher neutrophil count, but analysis of T-cell subsets showed no difference between the two groups. In peripheral blood, secretion of interleukin-2 (IL-2) after mitogenic stimulation was significantly diminished in the patients' group (p < 0.01), whereas values of IFN-α2, IL-6, IFN-γ and sIL-2R were comparable in both groups. IL-2 production correlated negatively with the mean annual dose of levodopa treatment and correlated significantly (p < 0.002) with amantadine uptake. Analysis of sex, age, duration of illness and other drug intake revealed no correlation with cytokine release. Our findings support the view that there is a selective abnormality in the immune repertoire of peripheral blood lymphocytes in patients suffering from PD, the reasons for which need to be explored.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Harald Klüter</name><affiliations><json:string>Institute of Immunology and Transfusion Medicine, University of Lübeck School of Medicine, Ratzeburger Allee 160, D-23538 Lübeck, Germany</json:string></affiliations></json:item><json:item><name>Peter Vieregge</name><affiliations><json:string>Clinic of Neurology, University of Lübeck School of Medicine, Lübeck, Germany</json:string></affiliations></json:item><json:item><name>Henning Stolze</name><affiliations><json:string>Clinic of Neurology, University of Lübeck School of Medicine, Lübeck, Germany</json:string></affiliations></json:item><json:item><name>Holger Kirchner</name><affiliations><json:string>Institute of Immunology and Transfusion Medicine, University of Lübeck School of Medicine, Ratzeburger Allee 160, D-23538 Lübeck, Germany</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Clinical section</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson disease immunology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson disease drug therapy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Lymphocyte analysis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Cytokine release</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Whole-blood assay</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Interleukin-2 analysis</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The pathogenesis of Parkinson's disease (PD) is largely unknown. Recently, several studies have presented evidence of an immunological dysfunction in patients suffering from PD. We studied the immune responsiveness of patients with idiopathic PD (n = 20) by investigation of the ability of peripheral blood mononuclear cells to produce cytokines after mitogenic stimulation in a whole blood assay. A group of age-related healthy blood donors served as control (n = 19). Additionally, white blood count, leukocyte differentiation and lymphocyte subtyping were performed. PD patients had a significantly higher neutrophil count, but analysis of T-cell subsets showed no difference between the two groups. In peripheral blood, secretion of interleukin-2 (IL-2) after mitogenic stimulation was significantly diminished in the patients' group (p > 0.01), whereas values of IFN-α2, IL-6, IFN-γ and sIL-2R were comparable in both groups. IL-2 production correlated negatively with the mean annual dose of levodopa treatment and correlated significantly (p > 0.002) with amantadine uptake. Analysis of sex, age, duration of illness and other drug intake revealed no correlation with cytokine release. Our findings support the view that there is a selective abnormality in the immune repertoire of peripheral blood lymphocytes in patients suffering from PD, the reasons for which need to be explored.</abstract><qualityIndicators><score>5.881</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612.28 x 792.28 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>7</keywordCount><abstractCharCount>1391</abstractCharCount><pdfWordCount>3421</pdfWordCount><pdfCharCount>22903</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>205</abstractWordCount></qualityIndicators><title>Defective production of interleukin-2 in patients with idiopathic Parkinson's disease</title><pii><json:string>0022-510X(95)00180-A</json:string></pii><genre><json:string>research-article</json:string></genre><serie><volume>79</volume><pages><last>2295</last><first>2291</first></pages><genre></genre><language><json:string>unknown</json:string></language><title>Proc. Natl. Acad. Sci. 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Tel.: (+49-451) 500-2840; Fax: (+49-451) 500-2857.</p></note><affiliation>Institute of Immunology and Transfusion Medicine, University of Lübeck School of Medicine, Ratzeburger Allee 160, D-23538 Lübeck, Germany</affiliation></author><author><persName><forename type="first">Peter</forename><surname>Vieregge</surname></persName><affiliation>Clinic of Neurology, University of Lübeck School of Medicine, Lübeck, Germany</affiliation></author><author><persName><forename type="first">Henning</forename><surname>Stolze</surname></persName><affiliation>Clinic of Neurology, University of Lübeck School of Medicine, Lübeck, Germany</affiliation></author><author><persName><forename type="first">Holger</forename><surname>Kirchner</surname></persName><affiliation>Institute of Immunology and Transfusion Medicine, University of Lübeck School of Medicine, Ratzeburger Allee 160, D-23538 Lübeck, Germany</affiliation></author></analytic><monogr><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="pISSN">0022-510X</idno><idno type="PII">S0022-510X(00)X0010-X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1995"></date><biblScope unit="volume">133</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="134">134</biblScope><biblScope unit="page" to="139">139</biblScope></imprint></monogr><idno type="istex">A6EE178C9040AB845E09B67F482DF61794DB68E7</idno><idno type="DOI">10.1016/0022-510X(95)00180-A</idno><idno type="PII">0022-510X(95)00180-A</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1995</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The pathogenesis of Parkinson's disease (PD) is largely unknown. Recently, several studies have presented evidence of an immunological dysfunction in patients suffering from PD. We studied the immune responsiveness of patients with idiopathic PD (n = 20) by investigation of the ability of peripheral blood mononuclear cells to produce cytokines after mitogenic stimulation in a whole blood assay. A group of age-related healthy blood donors served as control (n = 19). Additionally, white blood count, leukocyte differentiation and lymphocyte subtyping were performed. PD patients had a significantly higher neutrophil count, but analysis of T-cell subsets showed no difference between the two groups. In peripheral blood, secretion of interleukin-2 (IL-2) after mitogenic stimulation was significantly diminished in the patients' group (p < 0.01), whereas values of IFN-α2, IL-6, IFN-γ and sIL-2R were comparable in both groups. IL-2 production correlated negatively with the mean annual dose of levodopa treatment and correlated significantly (p < 0.002) with amantadine uptake. Analysis of sex, age, duration of illness and other drug intake revealed no correlation with cytokine release. Our findings support the view that there is a selective abnormality in the immune repertoire of peripheral blood lymphocytes in patients suffering from PD, the reasons for which need to be explored.</p></abstract><textClass><keywords scheme="keyword"><list><head>Article category</head><item><term>Clinical section</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson disease immunology</term></item><item><term>Parkinson disease drug therapy</term></item><item><term>Lymphocyte analysis</term></item><item><term>Cytokine release</term></item><item><term>Whole-blood assay</term></item><item><term>Interleukin-2 analysis</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1995-05-29">Registration</change><change when="1995-05-25">Modified</change><change when="1995">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>JNS</jid><aid>9500180A</aid><ce:pii>0022-510X(95)00180-A</ce:pii><ce:doi>10.1016/0022-510X(95)00180-A</ce:doi><ce:copyright type="unknown" year="1995"></ce:copyright><ce:doctopics><ce:doctopic><ce:text>Clinical section</ce:text></ce:doctopic></ce:doctopics></item-info><head><ce:dochead><ce:textfn>Research article</ce:textfn></ce:dochead><ce:title>Defective production of interleukin-2 in patients with idiopathic Parkinson's disease</ce:title><ce:author-group><ce:author><ce:given-name>Harald</ce:given-name><ce:surname>Klüter</ce:surname><ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Peter</ce:given-name><ce:surname>Vieregge</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Henning</ce:given-name><ce:surname>Stolze</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Holger</ce:given-name><ce:surname>Kirchner</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Institute of Immunology and Transfusion Medicine, University of Lübeck School of Medicine, Ratzeburger Allee 160, D-23538 Lübeck, Germany</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Clinic of Neurology, University of Lübeck School of Medicine, Lübeck, Germany</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Corresponding author. Tel.: (+49-451) 500-2840; Fax: (+49-451) 500-2857.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="30" month="12" year="1994"></ce:date-received><ce:date-revised day="25" month="5" year="1995"></ce:date-revised><ce:date-accepted day="29" month="5" year="1995"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>The pathogenesis of Parkinson's disease (PD) is largely unknown. Recently, several studies have presented evidence of an immunological dysfunction in patients suffering from PD. We studied the immune responsiveness of patients with idiopathic PD (<ce:italic>n</ce:italic> = 20) by investigation of the ability of peripheral blood mononuclear cells to produce cytokines after mitogenic stimulation in a whole blood assay. A group of age-related healthy blood donors served as control (<ce:italic>n</ce:italic> = 19). Additionally, white blood count, leukocyte differentiation and lymphocyte subtyping were performed. PD patients had a significantly higher neutrophil count, but analysis of T-cell subsets showed no difference between the two groups. In peripheral blood, secretion of interleukin-2 (IL-2) after mitogenic stimulation was significantly diminished in the patients' group (<ce:italic>p</ce:italic> < 0.01), whereas values of IFN-α2, IL-6, IFN-γ and sIL-2R were comparable in both groups. IL-2 production correlated negatively with the mean annual dose of levodopa treatment and correlated significantly (<ce:italic>p</ce:italic> < 0.002) with amantadine uptake. Analysis of sex, age, duration of illness and other drug intake revealed no correlation with cytokine release. Our findings support the view that there is a selective abnormality in the immune repertoire of peripheral blood lymphocytes in patients suffering from PD, the reasons for which need to be explored.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Parkinson disease immunology</ce:text></ce:keyword><ce:keyword><ce:text>Parkinson disease drug therapy</ce:text></ce:keyword><ce:keyword><ce:text>Lymphocyte analysis</ce:text></ce:keyword><ce:keyword><ce:text>Cytokine release</ce:text></ce:keyword><ce:keyword><ce:text>Whole-blood assay</ce:text></ce:keyword><ce:keyword><ce:text>Interleukin-2 analysis</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Defective production of interleukin-2 in patients with idiopathic Parkinson's disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Defective production of interleukin-2 in patients with idiopathic Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Harald</namePart><namePart type="family">Klüter</namePart><affiliation>Institute of Immunology and Transfusion Medicine, University of Lübeck School of Medicine, Ratzeburger Allee 160, D-23538 Lübeck, Germany</affiliation><description>Corresponding author. Tel.: (+49-451) 500-2840; Fax: (+49-451) 500-2857.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter</namePart><namePart type="family">Vieregge</namePart><affiliation>Clinic of Neurology, University of Lübeck School of Medicine, Lübeck, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Henning</namePart><namePart type="family">Stolze</namePart><affiliation>Clinic of Neurology, University of Lübeck School of Medicine, Lübeck, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Holger</namePart><namePart type="family">Kirchner</namePart><affiliation>Institute of Immunology and Transfusion Medicine, University of Lübeck School of Medicine, Ratzeburger Allee 160, D-23538 Lübeck, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1995</dateIssued><dateValid encoding="w3cdtf">1995-05-29</dateValid><dateModified encoding="w3cdtf">1995-05-25</dateModified><copyrightDate encoding="w3cdtf">1995</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">The pathogenesis of Parkinson's disease (PD) is largely unknown. Recently, several studies have presented evidence of an immunological dysfunction in patients suffering from PD. We studied the immune responsiveness of patients with idiopathic PD (n = 20) by investigation of the ability of peripheral blood mononuclear cells to produce cytokines after mitogenic stimulation in a whole blood assay. A group of age-related healthy blood donors served as control (n = 19). Additionally, white blood count, leukocyte differentiation and lymphocyte subtyping were performed. PD patients had a significantly higher neutrophil count, but analysis of T-cell subsets showed no difference between the two groups. In peripheral blood, secretion of interleukin-2 (IL-2) after mitogenic stimulation was significantly diminished in the patients' group (p < 0.01), whereas values of IFN-α2, IL-6, IFN-γ and sIL-2R were comparable in both groups. IL-2 production correlated negatively with the mean annual dose of levodopa treatment and correlated significantly (p < 0.002) with amantadine uptake. Analysis of sex, age, duration of illness and other drug intake revealed no correlation with cytokine release. Our findings support the view that there is a selective abnormality in the immune repertoire of peripheral blood lymphocytes in patients suffering from PD, the reasons for which need to be explored.</abstract><note type="content">Section title: Research article</note><subject><genre>Article category</genre><topic>Clinical section</topic></subject><subject><genre>Keywords</genre><topic>Parkinson disease immunology</topic><topic>Parkinson disease drug therapy</topic><topic>Lymphocyte analysis</topic><topic>Cytokine release</topic><topic>Whole-blood assay</topic><topic>Interleukin-2 analysis</topic></subject><relatedItem type="host"><titleInfo><title>Journal of the Neurological Sciences</title></titleInfo><titleInfo type="abbreviated"><title>JNS</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">199511</dateIssued></originInfo><identifier type="ISSN">0022-510X</identifier><identifier type="PII">S0022-510X(00)X0010-X</identifier><part><date>199511</date><detail type="volume"><number>133</number><caption>vol.</caption></detail><detail type="issue"><number>1–2</number><caption>no.</caption></detail><extent unit="issue pages"><start>1</start><end>209</end></extent><extent unit="pages"><start>134</start><end>139</end></extent></part></relatedItem><identifier type="istex">A6EE178C9040AB845E09B67F482DF61794DB68E7</identifier><identifier type="DOI">10.1016/0022-510X(95)00180-A</identifier><identifier type="PII">0022-510X(95)00180-A</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/A6EE178C9040AB845E09B67F482DF61794DB68E7/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</classCode><classCode scheme="WOS">NEUROIMAGING</classCode><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments></istex></record>Pour manipuler ce document sous Unix (Dilib)
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