Analysis of alloreactivity and intragraft cytokine profiles in living donor liver transplant recipients with graft acceptance
Identifieur interne : 002337 ( Istex/Corpus ); précédent : 002336; suivant : 002338Analysis of alloreactivity and intragraft cytokine profiles in living donor liver transplant recipients with graft acceptance
Auteurs : Mitsuhisa Takatsuki ; Shinji Uemoto ; Yukihiro Inomata ; Seisuke Sakamoto ; Michihiro Hayashi ; Mikiko Ueda ; Takashi Kanematsu ; Koichi TanakaSource :
- Transplant Immunology [ 0966-3274 ] ; 2001.
English descriptors
- KwdEn :
- CTLp, cytotoxic T lymphocyte precursors, Cytokine, EBV, Epstein-Barr virus., ELISA, enzyme-linked immunosorbent assay, HLA, human leukocyte antigen, IL, interleukin, INF γ, interferon γ, LDLT, living donor liver transplantation, Liver transplantation, MLR, mixed lymphocyte reaction, PBMNC, peripheral blood mononuclear cells, PTLD, posttransplant lymphoproliferative disorder, RT-PCR, reverse transcriptase-polymerase chain reaction, TNFα, tumor necrosis factor α, Th, T helper, Tolerance, dNTP, deoxy nucleoside triphosphate, dUTP, deoxy uridine triphosphate.
Abstract
Although some previous studies have indicated the possibility of immunosuppression withdrawal in clinical liver transplantation, the mechanism of graft acceptance is not clear. The aim of this study is to elucidate the alloreactivity against the donor and intragraft cytokine profiles in living donor liver transplant (LDLT) recipients with graft acceptance. In October 1999, we had 23 patients who survived without immunosuppression after LDLT with a median drug-free period of 25 months (range: 3–69 months). They consisted of six patients who were electively weaned by an elective weaning protocol and 17 either forcibly or accidentally weaned patients due to various causes but mainly due to infection. We evaluated the alloreactivity against the donor in these patients by a mixed lymphocyte reaction and intragraft cytokine profiles by real-time reverse transcriptase-polymerase chain reaction. The development of donor-specific hyporeactivity was observed in the patients with graft acceptance. The cytokine pattern in the supernatant of the culture medium revealed a down regulation of T helper (Th) 1 cytokine INF γ against the donor while no significant difference was seen in Th2 cytokine IL-10. Regarding the intragraft cytokine profiles, we could find no amplification of Th1 cytokines (IL-2, INF γ) and IL-4 while some of the patients revealed a gene expression of IL-10 with no significant difference from that of the normal, untransplanted liver specimen. In addition, no difference was observed in any other cytokines (IL-1β, IL-8, IL-15, TNFα) compared with those of the normal controls. We propose that the down regulation of Th1 cytokine is one possible mechanism of graft acceptance in LDLT recipients.
Url:
DOI: 10.1016/S0966-3274(01)00027-2
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Japan</mods:affiliation></affiliation></author><author><name sortKey="Uemoto, Shinji" sort="Uemoto, Shinji" uniqKey="Uemoto S" first="Shinji" last="Uemoto">Shinji Uemoto</name><affiliation><mods:affiliation>E-mail: ueshin@kuhp.kyoto-u.ac.jp</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</mods:affiliation></affiliation></author><author><name sortKey="Inomata, Yukihiro" sort="Inomata, Yukihiro" uniqKey="Inomata Y" first="Yukihiro" last="Inomata">Yukihiro Inomata</name><affiliation><mods:affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</mods:affiliation></affiliation></author><author><name sortKey="Sakamoto, Seisuke" sort="Sakamoto, Seisuke" uniqKey="Sakamoto S" first="Seisuke" last="Sakamoto">Seisuke Sakamoto</name><affiliation><mods:affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</mods:affiliation></affiliation></author><author><name sortKey="Hayashi, Michihiro" sort="Hayashi, Michihiro" uniqKey="Hayashi M" first="Michihiro" last="Hayashi">Michihiro Hayashi</name><affiliation><mods:affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</mods:affiliation></affiliation></author><author><name sortKey="Ueda, Mikiko" sort="Ueda, Mikiko" uniqKey="Ueda M" first="Mikiko" last="Ueda">Mikiko Ueda</name><affiliation><mods:affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</mods:affiliation></affiliation></author><author><name sortKey="Kanematsu, Takashi" sort="Kanematsu, Takashi" uniqKey="Kanematsu T" first="Takashi" last="Kanematsu">Takashi Kanematsu</name><affiliation><mods:affiliation>Department of Surgery II, 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triphosphate</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although some previous studies have indicated the possibility of immunosuppression withdrawal in clinical liver transplantation, the mechanism of graft acceptance is not clear. The aim of this study is to elucidate the alloreactivity against the donor and intragraft cytokine profiles in living donor liver transplant (LDLT) recipients with graft acceptance. In October 1999, we had 23 patients who survived without immunosuppression after LDLT with a median drug-free period of 25 months (range: 3–69 months). They consisted of six patients who were electively weaned by an elective weaning protocol and 17 either forcibly or accidentally weaned patients due to various causes but mainly due to infection. We evaluated the alloreactivity against the donor in these patients by a mixed lymphocyte reaction and intragraft cytokine profiles by real-time reverse transcriptase-polymerase chain reaction. The development of donor-specific hyporeactivity was observed in the patients with graft acceptance. The cytokine pattern in the supernatant of the culture medium revealed a down regulation of T helper (Th) 1 cytokine INF γ against the donor while no significant difference was seen in Th2 cytokine IL-10. Regarding the intragraft cytokine profiles, we could find no amplification of Th1 cytokines (IL-2, INF γ) and IL-4 while some of the patients revealed a gene expression of IL-10 with no significant difference from that of the normal, untransplanted liver specimen. In addition, no difference was observed in any other cytokines (IL-1β, IL-8, IL-15, TNFα) compared with those of the normal controls. We propose that the down regulation of Th1 cytokine is one possible mechanism of graft acceptance in LDLT recipients.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Mitsuhisa Takatsuki</name><affiliations><json:string>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</json:string></affiliations></json:item><json:item><name>Shinji Uemoto</name><affiliations><json:string>E-mail: ueshin@kuhp.kyoto-u.ac.jp</json:string><json:string>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</json:string></affiliations></json:item><json:item><name>Yukihiro Inomata</name><affiliations><json:string>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</json:string></affiliations></json:item><json:item><name>Seisuke Sakamoto</name><affiliations><json:string>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</json:string></affiliations></json:item><json:item><name>Michihiro Hayashi</name><affiliations><json:string>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</json:string></affiliations></json:item><json:item><name>Mikiko Ueda</name><affiliations><json:string>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</json:string></affiliations></json:item><json:item><name>Takashi Kanematsu</name><affiliations><json:string>Department of Surgery II, Nagasaki University, Nagasaki 852-8501, Japan</json:string></affiliations></json:item><json:item><name>Koichi Tanaka</name><affiliations><json:string>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Liver transplantation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Tolerance</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Cytokine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>LDLT, living donor liver transplantation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Th, T helper</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>IL, interleukin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>INF γ, interferon γ</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>TNFα, tumor necrosis factor α</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MLR, mixed lymphocyte reaction</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CTLp, cytotoxic T lymphocyte precursors</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>RT-PCR, reverse transcriptase-polymerase chain reaction</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PTLD, posttransplant lymphoproliferative disorder</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PBMNC, peripheral blood mononuclear cells</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>HLA, human leukocyte antigen</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>ELISA, enzyme-linked immunosorbent assay</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dNTP, deoxy nucleoside triphosphate</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dUTP, deoxy uridine triphosphate</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>EBV, Epstein-Barr virus.</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Although some previous studies have indicated the possibility of immunosuppression withdrawal in clinical liver transplantation, the mechanism of graft acceptance is not clear. The aim of this study is to elucidate the alloreactivity against the donor and intragraft cytokine profiles in living donor liver transplant (LDLT) recipients with graft acceptance. In October 1999, we had 23 patients who survived without immunosuppression after LDLT with a median drug-free period of 25 months (range: 3–69 months). They consisted of six patients who were electively weaned by an elective weaning protocol and 17 either forcibly or accidentally weaned patients due to various causes but mainly due to infection. We evaluated the alloreactivity against the donor in these patients by a mixed lymphocyte reaction and intragraft cytokine profiles by real-time reverse transcriptase-polymerase chain reaction. The development of donor-specific hyporeactivity was observed in the patients with graft acceptance. The cytokine pattern in the supernatant of the culture medium revealed a down regulation of T helper (Th) 1 cytokine INF γ against the donor while no significant difference was seen in Th2 cytokine IL-10. Regarding the intragraft cytokine profiles, we could find no amplification of Th1 cytokines (IL-2, INF γ) and IL-4 while some of the patients revealed a gene expression of IL-10 with no significant difference from that of the normal, untransplanted liver specimen. In addition, no difference was observed in any other cytokines (IL-1β, IL-8, IL-15, TNFα) compared with those of the normal controls. We propose that the down regulation of Th1 cytokine is one possible mechanism of graft acceptance in LDLT recipients.</abstract><qualityIndicators><score>7.687</score><pdfVersion>1.2</pdfVersion><pdfPageSize>595 x 794 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>18</keywordCount><abstractCharCount>1723</abstractCharCount><pdfWordCount>4687</pdfWordCount><pdfCharCount>30932</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>259</abstractWordCount></qualityIndicators><title>Analysis of alloreactivity and intragraft cytokine profiles in living donor liver transplant recipients with graft acceptance</title><pii><json:string>S0966-3274(01)00027-2</json:string></pii><genre><json:string>research-article</json:string></genre><host><volume>8</volume><pii><json:string>S0966-3274(00)X0004-4</json:string></pii><pages><last>286</last><first>279</first></pages><issn><json:string>0966-3274</json:string></issn><issue>4</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><title>Transplant Immunology</title><publicationDate>2001</publicationDate></host><categories><wos><json:string>IMMUNOLOGY</json:string><json:string>TRANSPLANTATION</json:string></wos></categories><publicationDate>2001</publicationDate><copyrightDate>2001</copyrightDate><doi><json:string>10.1016/S0966-3274(01)00027-2</json:string></doi><id>21854ED1BE3C152B383AF31B7AA6576817D1D6A9</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/21854ED1BE3C152B383AF31B7AA6576817D1D6A9/fulltext/pdf</uri></json:item><json:item><original>true</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/21854ED1BE3C152B383AF31B7AA6576817D1D6A9/fulltext/txt</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/21854ED1BE3C152B383AF31B7AA6576817D1D6A9/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/21854ED1BE3C152B383AF31B7AA6576817D1D6A9/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Analysis of alloreactivity and intragraft cytokine profiles in living donor liver transplant recipients with graft acceptance</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>2001</date></publicationStmt><notesStmt><note type="content">Fig. 1: Alloreactivity against the donors or third parties in MLR. HLA-unrelated individuals were used as third party control.</note><note type="content">Fig. 2: Concentration of Th1 (INF γ) or Th2 (IL-10) cytokines in the supernatant of culture medium in MLR. Assays were performed by standard ELISA.</note><note type="content">Fig. 3: Intragraft cytokine profiles in the liver specimen of control (•) and tolerance (▵) by real-time RT-PCR. Normal and untransplanted liver was used as control. NA indicated no amplification. The quantity was expressed relative to one of the samples which revealed the actual amplification.</note><note type="content">Table 1:</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Analysis of alloreactivity and intragraft cytokine profiles in living donor liver transplant recipients with graft acceptance</title><author><persName><forename type="first">Mitsuhisa</forename><surname>Takatsuki</surname></persName><affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</affiliation></author><author><persName><forename type="first">Shinji</forename><surname>Uemoto</surname></persName><email>ueshin@kuhp.kyoto-u.ac.jp</email><note type="correspondence"><p>Corresponding author. Tel. +81-75-751-4323; fax: +81-75-751-4348</p></note><affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</affiliation></author><author><persName><forename type="first">Yukihiro</forename><surname>Inomata</surname></persName><affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</affiliation></author><author><persName><forename type="first">Seisuke</forename><surname>Sakamoto</surname></persName><affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</affiliation></author><author><persName><forename type="first">Michihiro</forename><surname>Hayashi</surname></persName><affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</affiliation></author><author><persName><forename type="first">Mikiko</forename><surname>Ueda</surname></persName><affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</affiliation></author><author><persName><forename type="first">Takashi</forename><surname>Kanematsu</surname></persName><affiliation>Department of Surgery II, Nagasaki University, Nagasaki 852-8501, Japan</affiliation></author><author><persName><forename type="first">Koichi</forename><surname>Tanaka</surname></persName><affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</affiliation></author></analytic><monogr><title level="j">Transplant Immunology</title><title level="j" type="abbrev">TRIM</title><idno type="pISSN">0966-3274</idno><idno type="PII">S0966-3274(00)X0004-4</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001"></date><biblScope unit="volume">8</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="279">279</biblScope><biblScope unit="page" to="286">286</biblScope></imprint></monogr><idno type="istex">21854ED1BE3C152B383AF31B7AA6576817D1D6A9</idno><idno type="DOI">10.1016/S0966-3274(01)00027-2</idno><idno type="PII">S0966-3274(01)00027-2</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Although some previous studies have indicated the possibility of immunosuppression withdrawal in clinical liver transplantation, the mechanism of graft acceptance is not clear. The aim of this study is to elucidate the alloreactivity against the donor and intragraft cytokine profiles in living donor liver transplant (LDLT) recipients with graft acceptance. In October 1999, we had 23 patients who survived without immunosuppression after LDLT with a median drug-free period of 25 months (range: 3–69 months). They consisted of six patients who were electively weaned by an elective weaning protocol and 17 either forcibly or accidentally weaned patients due to various causes but mainly due to infection. We evaluated the alloreactivity against the donor in these patients by a mixed lymphocyte reaction and intragraft cytokine profiles by real-time reverse transcriptase-polymerase chain reaction. The development of donor-specific hyporeactivity was observed in the patients with graft acceptance. The cytokine pattern in the supernatant of the culture medium revealed a down regulation of T helper (Th) 1 cytokine INF γ against the donor while no significant difference was seen in Th2 cytokine IL-10. Regarding the intragraft cytokine profiles, we could find no amplification of Th1 cytokines (IL-2, INF γ) and IL-4 while some of the patients revealed a gene expression of IL-10 with no significant difference from that of the normal, untransplanted liver specimen. In addition, no difference was observed in any other cytokines (IL-1β, IL-8, IL-15, TNFα) compared with those of the normal controls. We propose that the down regulation of Th1 cytokine is one possible mechanism of graft acceptance in LDLT recipients.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Liver transplantation</term></item><item><term>Tolerance</term></item><item><term>Cytokine</term></item></list></keywords></textClass><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Abbreviations</head><item><term>LDLT, living donor liver transplantation</term></item><item><term>Th, T helper</term></item><item><term>IL, interleukin</term></item><item><term>INF γ, interferon γ</term></item><item><term>TNFα, tumor necrosis factor α</term></item><item><term>MLR, mixed lymphocyte reaction</term></item><item><term>CTLp, cytotoxic T lymphocyte precursors</term></item><item><term>RT-PCR, reverse transcriptase-polymerase chain reaction</term></item><item><term>PTLD, posttransplant lymphoproliferative disorder</term></item><item><term>PBMNC, peripheral blood mononuclear cells</term></item><item><term>HLA, human leukocyte antigen</term></item><item><term>ELISA, enzyme-linked immunosorbent assay</term></item><item><term>dNTP, deoxy nucleoside triphosphate</term></item><item><term>dUTP, deoxy uridine triphosphate</term></item><item><term>EBV, Epstein-Barr virus.</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2001-01-08">Registration</change><change when="2001">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: ce:floats; body; 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:entity SYSTEM="gr1" NDATA="IMAGE" name="gr1"></istex:entity><istex:entity SYSTEM="gr2" NDATA="IMAGE" name="gr2"></istex:entity><istex:entity SYSTEM="gr3" NDATA="IMAGE" name="gr3"></istex:entity></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>TRIM</jid><aid>30</aid><ce:pii>S0966-3274(01)00027-2</ce:pii><ce:doi>10.1016/S0966-3274(01)00027-2</ce:doi><ce:copyright type="full-transfer" year="2001">Elsevier Science B.V.</ce:copyright></item-info><head><ce:title>Analysis of alloreactivity and intragraft cytokine profiles in living donor liver transplant recipients with graft acceptance</ce:title><ce:author-group><ce:author><ce:given-name>Mitsuhisa</ce:given-name><ce:surname>Takatsuki</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Shinji</ce:given-name><ce:surname>Uemoto</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="CORR1">*</ce:cross-ref><ce:e-address>ueshin@kuhp.kyoto-u.ac.jp</ce:e-address></ce:author><ce:author><ce:given-name>Yukihiro</ce:given-name><ce:surname>Inomata</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Seisuke</ce:given-name><ce:surname>Sakamoto</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Michihiro</ce:given-name><ce:surname>Hayashi</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Mikiko</ce:given-name><ce:surname>Ueda</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Takashi</ce:given-name><ce:surname>Kanematsu</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Koichi</ce:given-name><ce:surname>Tanaka</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>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Surgery II, Nagasaki University, Nagasaki 852-8501, Japan</ce:textfn></ce:affiliation><ce:correspondence id="CORR1"><ce:label>*</ce:label><ce:text>Corresponding author. Tel. +81-75-751-4323; fax: +81-75-751-4348</ce:text></ce:correspondence></ce:author-group><ce:date-received day="21" month="12" year="2000"></ce:date-received><ce:date-accepted day="8" month="1" year="2001"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Although some previous studies have indicated the possibility of immunosuppression withdrawal in clinical liver transplantation, the mechanism of graft acceptance is not clear. The aim of this study is to elucidate the alloreactivity against the donor and intragraft cytokine profiles in living donor liver transplant (LDLT) recipients with graft acceptance. In October 1999, we had 23 patients who survived without immunosuppression after LDLT with a median drug-free period of 25 months (range: 3–69 months). They consisted of six patients who were electively weaned by an elective weaning protocol and 17 either forcibly or accidentally weaned patients due to various causes but mainly due to infection. We evaluated the alloreactivity against the donor in these patients by a mixed lymphocyte reaction and intragraft cytokine profiles by real-time reverse transcriptase-polymerase chain reaction. The development of donor-specific hyporeactivity was observed in the patients with graft acceptance. The cytokine pattern in the supernatant of the culture medium revealed a down regulation of T helper (Th) 1 cytokine INF γ against the donor while no significant difference was seen in Th2 cytokine IL-10. Regarding the intragraft cytokine profiles, we could find no amplification of Th1 cytokines (IL-2, INF γ) and IL-4 while some of the patients revealed a gene expression of IL-10 with no significant difference from that of the normal, untransplanted liver specimen. In addition, no difference was observed in any other cytokines (IL-1β, IL-8, IL-15, TNFα) compared with those of the normal controls. We propose that the down regulation of Th1 cytokine is one possible mechanism of graft acceptance in LDLT recipients.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Liver transplantation</ce:text></ce:keyword><ce:keyword><ce:text>Tolerance</ce:text></ce:keyword><ce:keyword><ce:text>Cytokine</ce:text></ce:keyword></ce:keywords><ce:keywords class="abr"><ce:section-title>Abbreviations</ce:section-title><ce:keyword><ce:text>LDLT, living donor liver transplantation</ce:text></ce:keyword><ce:keyword><ce:text>Th, T helper</ce:text></ce:keyword><ce:keyword><ce:text>IL, interleukin</ce:text></ce:keyword><ce:keyword><ce:text>INF γ, interferon γ</ce:text></ce:keyword><ce:keyword><ce:text>TNFα, tumor necrosis factor α</ce:text></ce:keyword><ce:keyword><ce:text>MLR, mixed lymphocyte reaction</ce:text></ce:keyword><ce:keyword><ce:text>CTLp, cytotoxic T lymphocyte precursors</ce:text></ce:keyword><ce:keyword><ce:text>RT-PCR, reverse transcriptase-polymerase chain reaction</ce:text></ce:keyword><ce:keyword><ce:text>PTLD, posttransplant lymphoproliferative disorder</ce:text></ce:keyword><ce:keyword><ce:text>PBMNC, peripheral blood mononuclear cells</ce:text></ce:keyword><ce:keyword><ce:text>HLA, human leukocyte antigen</ce:text></ce:keyword><ce:keyword><ce:text>ELISA, enzyme-linked immunosorbent assay</ce:text></ce:keyword><ce:keyword><ce:text>dNTP, deoxy nucleoside triphosphate</ce:text></ce:keyword><ce:keyword><ce:text>dUTP, deoxy uridine triphosphate</ce:text></ce:keyword><ce:keyword><ce:text>EBV, Epstein-Barr virus.</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Analysis of alloreactivity and intragraft cytokine profiles in living donor liver transplant recipients with graft acceptance</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Analysis of alloreactivity and intragraft cytokine profiles in living donor liver transplant recipients with graft acceptance</title></titleInfo><name type="personal"><namePart type="given">Mitsuhisa</namePart><namePart type="family">Takatsuki</namePart><affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shinji</namePart><namePart type="family">Uemoto</namePart><affiliation>E-mail: ueshin@kuhp.kyoto-u.ac.jp</affiliation><affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</affiliation><description>Corresponding author. Tel. +81-75-751-4323; fax: +81-75-751-4348</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yukihiro</namePart><namePart type="family">Inomata</namePart><affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Seisuke</namePart><namePart type="family">Sakamoto</namePart><affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michihiro</namePart><namePart type="family">Hayashi</namePart><affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mikiko</namePart><namePart type="family">Ueda</namePart><affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Takashi</namePart><namePart type="family">Kanematsu</namePart><affiliation>Department of Surgery II, Nagasaki University, Nagasaki 852-8501, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Koichi</namePart><namePart type="family">Tanaka</namePart><affiliation>Department of Transplantation and Immunology, Kyoto University, 54 Kawara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, 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">2001</dateIssued><dateValid encoding="w3cdtf">2001-01-08</dateValid><copyrightDate encoding="w3cdtf">2001</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">Although some previous studies have indicated the possibility of immunosuppression withdrawal in clinical liver transplantation, the mechanism of graft acceptance is not clear. The aim of this study is to elucidate the alloreactivity against the donor and intragraft cytokine profiles in living donor liver transplant (LDLT) recipients with graft acceptance. In October 1999, we had 23 patients who survived without immunosuppression after LDLT with a median drug-free period of 25 months (range: 3–69 months). They consisted of six patients who were electively weaned by an elective weaning protocol and 17 either forcibly or accidentally weaned patients due to various causes but mainly due to infection. We evaluated the alloreactivity against the donor in these patients by a mixed lymphocyte reaction and intragraft cytokine profiles by real-time reverse transcriptase-polymerase chain reaction. The development of donor-specific hyporeactivity was observed in the patients with graft acceptance. The cytokine pattern in the supernatant of the culture medium revealed a down regulation of T helper (Th) 1 cytokine INF γ against the donor while no significant difference was seen in Th2 cytokine IL-10. Regarding the intragraft cytokine profiles, we could find no amplification of Th1 cytokines (IL-2, INF γ) and IL-4 while some of the patients revealed a gene expression of IL-10 with no significant difference from that of the normal, untransplanted liver specimen. In addition, no difference was observed in any other cytokines (IL-1β, IL-8, IL-15, TNFα) compared with those of the normal controls. We propose that the down regulation of Th1 cytokine is one possible mechanism of graft acceptance in LDLT recipients.</abstract><note type="content">Fig. 1: Alloreactivity against the donors or third parties in MLR. HLA-unrelated individuals were used as third party control.</note><note type="content">Fig. 2: Concentration of Th1 (INF γ) or Th2 (IL-10) cytokines in the supernatant of culture medium in MLR. Assays were performed by standard ELISA.</note><note type="content">Fig. 3: Intragraft cytokine profiles in the liver specimen of control (•) and tolerance (▵) by real-time RT-PCR. Normal and untransplanted liver was used as control. NA indicated no amplification. The quantity was expressed relative to one of the samples which revealed the actual amplification.</note><note type="content">Table 1: </note><subject lang="en"><genre>Keywords</genre><topic>Liver transplantation</topic><topic>Tolerance</topic><topic>Cytokine</topic></subject><subject lang="en"><genre>Abbreviations</genre><topic>LDLT, living donor liver transplantation</topic><topic>Th, T helper</topic><topic>IL, interleukin</topic><topic>INF γ, interferon γ</topic><topic>TNFα, tumor necrosis factor α</topic><topic>MLR, mixed lymphocyte reaction</topic><topic>CTLp, cytotoxic T lymphocyte precursors</topic><topic>RT-PCR, reverse transcriptase-polymerase chain reaction</topic><topic>PTLD, posttransplant lymphoproliferative disorder</topic><topic>PBMNC, peripheral blood mononuclear cells</topic><topic>HLA, human leukocyte antigen</topic><topic>ELISA, enzyme-linked immunosorbent assay</topic><topic>dNTP, deoxy nucleoside triphosphate</topic><topic>dUTP, deoxy uridine triphosphate</topic><topic>EBV, Epstein-Barr virus.</topic></subject><relatedItem type="host"><titleInfo><title>Transplant Immunology</title></titleInfo><titleInfo type="abbreviated"><title>TRIM</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">200102</dateIssued></originInfo><identifier type="ISSN">0966-3274</identifier><identifier type="PII">S0966-3274(00)X0004-4</identifier><part><date>200102</date><detail type="volume"><number>8</number><caption>vol.</caption></detail><detail type="issue"><number>4</number><caption>no.</caption></detail><extent unit="issue pages"><start>219</start><end>298</end></extent><extent unit="pages"><start>279</start><end>286</end></extent></part></relatedItem><identifier type="istex">21854ED1BE3C152B383AF31B7AA6576817D1D6A9</identifier><identifier type="DOI">10.1016/S0966-3274(01)00027-2</identifier><identifier type="PII">S0966-3274(01)00027-2</identifier><accessCondition type="use and reproduction" contentType="">© 2001Elsevier Science B.V.</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>Elsevier Science B.V., ©2001</recordOrigin></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/21854ED1BE3C152B383AF31B7AA6576817D1D6A9/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">IMMUNOLOGY</classCode><classCode scheme="WOS">TRANSPLANTATION</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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