Characterization of adherent T cells to human endothelial cells in patients with HTLV-I-associated myelopathy
Identifieur interne : 001929 ( Istex/Corpus ); précédent : 001928; suivant : 001930Characterization of adherent T cells to human endothelial cells in patients with HTLV-I-associated myelopathy
Auteurs : Katsuhiro Ichinose ; Tatsufumi Nakamura ; Yoshihiro Nishiura ; Kunihiko Nagasato ; Kiyosumi Ohishi ; Hiroko Watanabe ; Akira Fujita ; Ken-Ichi Kurouji ; Mitsuhiro Tsujihata ; Shigenobu NagatakiSource :
- Journal of the Neurological Sciences [ 0022-510X ] ; 1993.
Abstract
To clarify the phenomenon of increased adherence of T cells to endothelial cells (EC) in patients with HTLV-I-associated myelopathy (HAM), we determined the surface markers and expression of lymphocyte function antigen-1 (LFA-1) in T cells adherent or nonadherent to EC. The percentage of activated or HLA-DR+ T cells and the expression of LFA-1 in the adherent cell population were significantly higher than those in the nonadherent cell population. Moreover, the CD4 to CD8 ratio of the HLA-DR+ cells in the EC-adherent T cells was significantly higher than that in the nonadherent cells. Collectively, these results indicate that increased adherence of T cells to EC in HAM patients is based on the increase of activated T cells with high density LFA-1 expression in the peripheral blood. Moreover, CD4+ HLA-DR+ cells exhibited more adhesive activity to EC than CD8+ HLA-DR+ cells, suggesting that activated CD4+ cells, rather than activated CD8+ cells, may be important as the first trigger for T cell-infiltration to the central nervous system in the immunopathogenesis of HAM.
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DOI: 10.1016/0022-510X(94)90299-2
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Tel.: 81-958-47-2111, ext. 2800; Fax: 81-958-43-0255.</mods:affiliation></affiliation><affiliation><mods:affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:81E6945445416C1C10BD95A60BF665B0C6756451</idno><date when="1994" year="1994">1994</date><idno type="doi">10.1016/0022-510X(94)90299-2</idno><idno type="url">https://api.istex.fr/document/81E6945445416C1C10BD95A60BF665B0C6756451/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001929</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Characterization of adherent T cells to human endothelial cells in patients with HTLV-I-associated myelopathy</title><author><name sortKey="Ichinose, Katsuhiro" sort="Ichinose, Katsuhiro" uniqKey="Ichinose K" first="Katsuhiro" last="Ichinose">Katsuhiro Ichinose</name><affiliation><mods:affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</mods:affiliation></affiliation></author><author><name sortKey="Nakamura, Tatsufumi" sort="Nakamura, Tatsufumi" uniqKey="Nakamura T" first="Tatsufumi" last="Nakamura">Tatsufumi Nakamura</name><affiliation><mods:affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</mods:affiliation></affiliation></author><author><name sortKey="Nishiura, Yoshihiro" sort="Nishiura, Yoshihiro" uniqKey="Nishiura Y" first="Yoshihiro" last="Nishiura">Yoshihiro Nishiura</name><affiliation><mods:affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</mods:affiliation></affiliation></author><author><name sortKey="Nagasato, Kunihiko" sort="Nagasato, Kunihiko" uniqKey="Nagasato K" first="Kunihiko" last="Nagasato">Kunihiko Nagasato</name><affiliation><mods:affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</mods:affiliation></affiliation></author><author><name sortKey="Ohishi, Kiyosumi" sort="Ohishi, Kiyosumi" uniqKey="Ohishi K" first="Kiyosumi" last="Ohishi">Kiyosumi Ohishi</name><affiliation><mods:affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</mods:affiliation></affiliation></author><author><name sortKey="Watanabe, Hiroko" sort="Watanabe, Hiroko" uniqKey="Watanabe H" first="Hiroko" last="Watanabe">Hiroko Watanabe</name><affiliation><mods:affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</mods:affiliation></affiliation></author><author><name sortKey="Fujita, Akira" sort="Fujita, Akira" uniqKey="Fujita A" first="Akira" last="Fujita">Akira Fujita</name><affiliation><mods:affiliation>Nagasaki Atomic Bomb Hospital, Japan Red Cross, Nagasaki, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kurouji, Ken Ichi" sort="Kurouji, Ken Ichi" uniqKey="Kurouji K" first="Ken-Ichi" last="Kurouji">Ken-Ichi Kurouji</name><affiliation><mods:affiliation>Nagasaki Atomic Bomb Hospital, Japan Red Cross, Nagasaki, Japan</mods:affiliation></affiliation></author><author><name sortKey="Tsujihata, Mitsuhiro" sort="Tsujihata, Mitsuhiro" uniqKey="Tsujihata M" first="Mitsuhiro" last="Tsujihata">Mitsuhiro Tsujihata</name><affiliation><mods:affiliation>School of Allied Medicine, Nagasaki University, Nagasaki, Japan</mods:affiliation></affiliation></author><author><name sortKey="Nagataki, Shigenobu" sort="Nagataki, Shigenobu" uniqKey="Nagataki S" first="Shigenobu" last="Nagataki">Shigenobu Nagataki</name><affiliation><mods:affiliation>Corresponding author. Tel.: 81-958-47-2111, ext. 2800; Fax: 81-958-43-0255.</mods:affiliation></affiliation><affiliation><mods:affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="ISSN">0022-510X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1993">1993</date><biblScope unit="volume">122</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="204">204</biblScope><biblScope unit="page" to="209">209</biblScope></imprint><idno type="ISSN">0022-510X</idno></series><idno type="istex">81E6945445416C1C10BD95A60BF665B0C6756451</idno><idno type="DOI">10.1016/0022-510X(94)90299-2</idno><idno type="PII">0022-510X(94)90299-2</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-510X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To clarify the phenomenon of increased adherence of T cells to endothelial cells (EC) in patients with HTLV-I-associated myelopathy (HAM), we determined the surface markers and expression of lymphocyte function antigen-1 (LFA-1) in T cells adherent or nonadherent to EC. The percentage of activated or HLA-DR+ T cells and the expression of LFA-1 in the adherent cell population were significantly higher than those in the nonadherent cell population. Moreover, the CD4 to CD8 ratio of the HLA-DR+ cells in the EC-adherent T cells was significantly higher than that in the nonadherent cells. Collectively, these results indicate that increased adherence of T cells to EC in HAM patients is based on the increase of activated T cells with high density LFA-1 expression in the peripheral blood. Moreover, CD4+ HLA-DR+ cells exhibited more adhesive activity to EC than CD8+ HLA-DR+ cells, suggesting that activated CD4+ cells, rather than activated CD8+ cells, may be important as the first trigger for T cell-infiltration to the central nervous system in the immunopathogenesis of HAM.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Katsuhiro Ichinose</name><affiliations><json:string>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</json:string></affiliations></json:item><json:item><name>Tatsufumi Nakamura</name><affiliations><json:string>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</json:string></affiliations></json:item><json:item><name>Yoshihiro Nishiura</name><affiliations><json:string>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</json:string></affiliations></json:item><json:item><name>Kunihiko Nagasato</name><affiliations><json:string>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</json:string></affiliations></json:item><json:item><name>Kiyosumi Ohishi</name><affiliations><json:string>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</json:string></affiliations></json:item><json:item><name>Hiroko Watanabe</name><affiliations><json:string>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</json:string></affiliations></json:item><json:item><name>Akira Fujita</name><affiliations><json:string>Nagasaki Atomic Bomb Hospital, Japan Red Cross, Nagasaki, Japan</json:string></affiliations></json:item><json:item><name>Ken-ichi Kurouji</name><affiliations><json:string>Nagasaki Atomic Bomb Hospital, Japan Red Cross, Nagasaki, Japan</json:string></affiliations></json:item><json:item><name>Mitsuhiro Tsujihata</name><affiliations><json:string>School of Allied Medicine, Nagasaki University, Nagasaki, Japan</json:string></affiliations></json:item><json:item><name>Shigenobu Nagataki,</name><affiliations><json:string>Corresponding author. Tel.: 81-958-47-2111, ext. 2800; Fax: 81-958-43-0255.</json:string><json:string>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>HTLV-I-associated myelopathy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>T cell-endothelial cell adhesion</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Adhesion molecule</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Activated T cells</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>T cell subset</value></json:item></subject><language><json:string>eng</json:string></language><abstract>To clarify the phenomenon of increased adherence of T cells to endothelial cells (EC) in patients with HTLV-I-associated myelopathy (HAM), we determined the surface markers and expression of lymphocyte function antigen-1 (LFA-1) in T cells adherent or nonadherent to EC. The percentage of activated or HLA-DR+ T cells and the expression of LFA-1 in the adherent cell population were significantly higher than those in the nonadherent cell population. Moreover, the CD4 to CD8 ratio of the HLA-DR+ cells in the EC-adherent T cells was significantly higher than that in the nonadherent cells. Collectively, these results indicate that increased adherence of T cells to EC in HAM patients is based on the increase of activated T cells with high density LFA-1 expression in the peripheral blood. Moreover, CD4+ HLA-DR+ cells exhibited more adhesive activity to EC than CD8+ HLA-DR+ cells, suggesting that activated CD4+ cells, rather than activated CD8+ cells, may be important as the first trigger for T cell-infiltration to the central nervous system in the immunopathogenesis of HAM.</abstract><qualityIndicators><score>6.053</score><pdfVersion>1.2</pdfVersion><pdfPageSize>576 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1082</abstractCharCount><pdfWordCount>4025</pdfWordCount><pdfCharCount>18416</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>169</abstractWordCount></qualityIndicators><title>Characterization of adherent T cells to human endothelial cells in patients with HTLV-I-associated 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uri="https://api.istex.fr/document/81E6945445416C1C10BD95A60BF665B0C6756451/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Characterization of adherent T cells to human endothelial cells in patients with HTLV-I-associated myelopathy</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>1994</date></publicationStmt><notesStmt><note type="content">Section title: Research article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Characterization of adherent T cells to human endothelial cells in patients with HTLV-I-associated myelopathy</title><author><persName><forename type="first">Katsuhiro</forename><surname>Ichinose</surname></persName><affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</affiliation></author><author><persName><forename type="first">Tatsufumi</forename><surname>Nakamura</surname></persName><affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</affiliation></author><author><persName><forename type="first">Yoshihiro</forename><surname>Nishiura</surname></persName><affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</affiliation></author><author><persName><forename type="first">Kunihiko</forename><surname>Nagasato</surname></persName><affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</affiliation></author><author><persName><forename type="first">Kiyosumi</forename><surname>Ohishi</surname></persName><affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</affiliation></author><author><persName><forename type="first">Hiroko</forename><surname>Watanabe</surname></persName><affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</affiliation></author><author><persName><forename type="first">Akira</forename><surname>Fujita</surname></persName><affiliation>Nagasaki Atomic Bomb Hospital, Japan Red Cross, Nagasaki, Japan</affiliation></author><author><persName><forename type="first">Ken-ichi</forename><surname>Kurouji</surname></persName><affiliation>Nagasaki Atomic Bomb Hospital, Japan Red Cross, Nagasaki, Japan</affiliation></author><author><persName><forename type="first">Mitsuhiro</forename><surname>Tsujihata</surname></persName><affiliation>School of Allied Medicine, Nagasaki University, Nagasaki, Japan</affiliation></author><author><persName><forename type="first">Shigenobu</forename><surname>Nagataki,</surname></persName><affiliation>Corresponding author. Tel.: 81-958-47-2111, ext. 2800; Fax: 81-958-43-0255.</affiliation><affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</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)X0366-8</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1993"></date><biblScope unit="volume">122</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="204">204</biblScope><biblScope unit="page" to="209">209</biblScope></imprint></monogr><idno type="istex">81E6945445416C1C10BD95A60BF665B0C6756451</idno><idno type="DOI">10.1016/0022-510X(94)90299-2</idno><idno type="PII">0022-510X(94)90299-2</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1994</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>To clarify the phenomenon of increased adherence of T cells to endothelial cells (EC) in patients with HTLV-I-associated myelopathy (HAM), we determined the surface markers and expression of lymphocyte function antigen-1 (LFA-1) in T cells adherent or nonadherent to EC. The percentage of activated or HLA-DR+ T cells and the expression of LFA-1 in the adherent cell population were significantly higher than those in the nonadherent cell population. Moreover, the CD4 to CD8 ratio of the HLA-DR+ cells in the EC-adherent T cells was significantly higher than that in the nonadherent cells. Collectively, these results indicate that increased adherence of T cells to EC in HAM patients is based on the increase of activated T cells with high density LFA-1 expression in the peripheral blood. Moreover, CD4+ HLA-DR+ cells exhibited more adhesive activity to EC than CD8+ HLA-DR+ cells, suggesting that activated CD4+ cells, rather than activated CD8+ cells, may be important as the first trigger for T cell-infiltration to the central nervous system in the immunopathogenesis of HAM.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>HTLV-I-associated myelopathy</term></item><item><term>T cell-endothelial cell adhesion</term></item><item><term>Adhesion molecule</term></item><item><term>Activated T cells</term></item><item><term>T cell subset</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1993-09-27">Registration</change><change when="1993-09-17">Modified</change><change when="1993">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>94902992</aid><ce:pii>0022-510X(94)90299-2</ce:pii><ce:doi>10.1016/0022-510X(94)90299-2</ce:doi><ce:copyright type="unknown" year="1994"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Research article</ce:textfn></ce:dochead><ce:title>Characterization of adherent T cells to human endothelial cells in patients with HTLV-I-associated myelopathy</ce:title><ce:author-group><ce:author><ce:given-name>Katsuhiro</ce:given-name><ce:surname>Ichinose</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Tatsufumi</ce:given-name><ce:surname>Nakamura</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Yoshihiro</ce:given-name><ce:surname>Nishiura</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Kunihiko</ce:given-name><ce:surname>Nagasato</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Kiyosumi</ce:given-name><ce:surname>Ohishi</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Hiroko</ce:given-name><ce:surname>Watanabe</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Akira</ce:given-name><ce:surname>Fujita</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>2</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Ken-ichi</ce:given-name><ce:surname>Kurouji</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>2</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Mitsuhiro</ce:given-name><ce:surname>Tsujihata</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>3</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Shigenobu</ce:given-name><ce:surname>Nagataki,</ce:surname><ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Nagasaki Atomic Bomb Hospital, Japan Red Cross, Nagasaki, Japan</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>c</ce:label><ce:textfn>School of Allied Medicine, Nagasaki University, Nagasaki, Japan</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Corresponding author. Tel.: 81-958-47-2111, ext. 2800; Fax: 81-958-43-0255.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="28" month="6" year="1993"></ce:date-received><ce:date-revised day="17" month="9" year="1993"></ce:date-revised><ce:date-accepted day="27" month="9" year="1993"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>To clarify the phenomenon of increased adherence of T cells to endothelial cells (EC) in patients with HTLV-I-associated myelopathy (HAM), we determined the surface markers and expression of lymphocyte function antigen-1 (LFA-1) in T cells adherent or nonadherent to EC. The percentage of activated or HLA-DR<ce:sup>+</ce:sup> T cells and the expression of LFA-1 in the adherent cell population were significantly higher than those in the nonadherent cell population. Moreover, the CD4 to CD8 ratio of the HLA-DR<ce:sup>+</ce:sup> cells in the EC-adherent T cells was significantly higher than that in the nonadherent cells. Collectively, these results indicate that increased adherence of T cells to EC in HAM patients is based on the increase of activated T cells with high density LFA-1 expression in the peripheral blood. Moreover, CD4<ce:sup>+</ce:sup> HLA-DR<ce:sup>+</ce:sup> cells exhibited more adhesive activity to EC than CD8<ce:sup>+</ce:sup> HLA-DR<ce:sup>+</ce:sup> cells, suggesting that activated CD4<ce:sup>+</ce:sup> cells, rather than activated CD8<ce:sup>+</ce:sup> cells, may be important as the first trigger for T cell-infiltration to the central nervous system in the immunopathogenesis of HAM.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>HTLV-I-associated myelopathy</ce:text></ce:keyword><ce:keyword><ce:text>T cell-endothelial cell adhesion</ce:text></ce:keyword><ce:keyword><ce:text>Adhesion molecule</ce:text></ce:keyword><ce:keyword><ce:text>Activated T cells</ce:text></ce:keyword><ce:keyword><ce:text>T cell subset</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Characterization of adherent T cells to human endothelial cells in patients with HTLV-I-associated myelopathy</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Characterization of adherent T cells to human endothelial cells in patients with HTLV-I-associated myelopathy</title></titleInfo><name type="personal"><namePart type="given">Katsuhiro</namePart><namePart type="family">Ichinose</namePart><affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tatsufumi</namePart><namePart type="family">Nakamura</namePart><affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yoshihiro</namePart><namePart type="family">Nishiura</namePart><affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kunihiko</namePart><namePart type="family">Nagasato</namePart><affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kiyosumi</namePart><namePart type="family">Ohishi</namePart><affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hiroko</namePart><namePart type="family">Watanabe</namePart><affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Akira</namePart><namePart type="family">Fujita</namePart><affiliation>Nagasaki Atomic Bomb Hospital, Japan Red Cross, Nagasaki, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ken-ichi</namePart><namePart type="family">Kurouji</namePart><affiliation>Nagasaki Atomic Bomb Hospital, Japan Red Cross, Nagasaki, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mitsuhiro</namePart><namePart type="family">Tsujihata</namePart><affiliation>School of Allied Medicine, Nagasaki University, Nagasaki, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shigenobu</namePart><namePart type="family">Nagataki,</namePart><affiliation>Corresponding author. Tel.: 81-958-47-2111, ext. 2800; Fax: 81-958-43-0255.</affiliation><affiliation>First Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan</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">1993</dateIssued><dateValid encoding="w3cdtf">1993-09-27</dateValid><dateModified encoding="w3cdtf">1993-09-17</dateModified><copyrightDate encoding="w3cdtf">1994</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">To clarify the phenomenon of increased adherence of T cells to endothelial cells (EC) in patients with HTLV-I-associated myelopathy (HAM), we determined the surface markers and expression of lymphocyte function antigen-1 (LFA-1) in T cells adherent or nonadherent to EC. The percentage of activated or HLA-DR+ T cells and the expression of LFA-1 in the adherent cell population were significantly higher than those in the nonadherent cell population. Moreover, the CD4 to CD8 ratio of the HLA-DR+ cells in the EC-adherent T cells was significantly higher than that in the nonadherent cells. Collectively, these results indicate that increased adherence of T cells to EC in HAM patients is based on the increase of activated T cells with high density LFA-1 expression in the peripheral blood. Moreover, CD4+ HLA-DR+ cells exhibited more adhesive activity to EC than CD8+ HLA-DR+ cells, suggesting that activated CD4+ cells, rather than activated CD8+ cells, may be important as the first trigger for T cell-infiltration to the central nervous system in the immunopathogenesis of HAM.</abstract><note type="content">Section title: Research article</note><subject><genre>Keywords</genre><topic>HTLV-I-associated myelopathy</topic><topic>T cell-endothelial cell adhesion</topic><topic>Adhesion molecule</topic><topic>Activated T cells</topic><topic>T cell subset</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">199404</dateIssued></originInfo><identifier type="ISSN">0022-510X</identifier><identifier type="PII">S0022-510X(00)X0366-8</identifier><part><date>199404</date><detail type="volume"><number>122</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue pages"><start>127</start><end>253</end></extent><extent unit="pages"><start>204</start><end>209</end></extent></part></relatedItem><identifier type="istex">81E6945445416C1C10BD95A60BF665B0C6756451</identifier><identifier type="DOI">10.1016/0022-510X(94)90299-2</identifier><identifier type="PII">0022-510X(94)90299-2</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/81E6945445416C1C10BD95A60BF665B0C6756451/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><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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