Autoimmune-Mediated Vasculopathy
Identifieur interne : 000889 ( Istex/Corpus ); précédent : 000888; suivant : 000890Autoimmune-Mediated Vasculopathy
Auteurs : Weiran Chen ; Christopher J. Thoburn ; Yuji Miura ; Matthias Sommer ; Ralph Hruban ; Zhiping Qian ; William Baldwin ; Allan D. HessSource :
- Clinical Immunology [ 1521-6616 ] ; 2001.
English descriptors
- KwdEn :
- Teeft :
- Acute phase, Acute response, Adoptive, Adoptive transfer, Allograft, Allograft rejection, Assay, Atherosclerosis, Autoaggression, Autoimmune, Autoimmune recognition, Autoimmune vasculopathy, Autologous, Autoreactive, Bone marrow transplant, Cdr3, Cdr3 size, Cell repertoire, Chloroquine, Chloroquine treatment, Chronic allograft rejection, Chronic gvhd, Chronic phases, Chronic rejection, Chronic sgvhd, Clonal, Clonal expansion model, Control template, Control template signals, Cyclosporine, Cytokine, Cytokine mrna transcripts, Determinant, Effector, Effector spleen cells, Endothelial, Endothelial cells, Endothelialitis, Endothelium, Graft, Graft atherosclerosis, Graft vasculopathy, Grafted, Grafted heart, Grafted hearts, Grafted tissue, Growth factor beta, Gvhd, Heart graft, Heart grafts, Heart transplantation, Hess, Immunol, Initial onset, Invariant chain, Lesion, Lymphocyte, Major histocompatibility, Medial, Medial wall, Mrna, Mrna transcripts, Neointima, Neointima formation, Nontransplanted, Nontransplanted heart, Normal mouse serum, Prebleed rabbit, Present studies, Recent studies, Receptor, Sgvhd, Sgvhd effector, Sgvhd effector lymphocytes, Subset, Syngeneic, Syngeneic disease, Syngeneic heart graft, Syngeneic heart grafts, Syngeneic heart transplantation, Target antigen, Target cells, Transplant, Transplantation, Upregulation, Vascular, Vascular disease, Vascular endothelium, Vascular lesions, Vasculopathy.
Abstract
Abstract: The use of the immunosuppressive drug cyclosporine A (CsA) in solid organ transplantation can be associated with the development of vasculopathy as part of the complex immune response involved in chronic rejection, including autoimmune recognition. Although CsA can directly affect endothelial cells, this drug alters the T cell repertoire promoting autoimmune recognition. The present studies evaluated the ability of CsA-induced autoreactive T cells to mediate vascular lesions in syngeneic heart grafts. Graft vasculopathy developed in syngeneic heart grafts following either the primary induction of autoimmunity with CsA or the adoptive transfer of CsA-induced autoreactive T cells. Initially, an inflammatory response occurred in the medial wall of the small arterial vessels, accompanied by a perivascular lymphocytic infiltrate (including a lymphocytic infiltrate into the myocardium), followed by progression of vascular disease with endothelial cell proliferation. The development and progression of vascular disease correlated with the cytokine profile of the infiltrating lymphocytes with type 1 cytokines detected early and type 2 cytokines detected as the disease progressed. Initiation of this response correlated with upregulation of the target antigen recognized by the CsA-induced autoreactive T cells, the MHC class II–invariant chain peptide complex. This antigen complex, when upregulated on endothelial cells by interferon, allowed effective targeting by the autoreactive T lymphocytes. Strategies to inhibit the upregulation of MHC class II antigens by treatment of the recipients with chloroquine truncated the disease process. The results of these studies suggest that CsA-induced autoreactive mechanisms can contribute to the development of graft vasculopathy.
Url:
DOI: 10.1006/clim.2001.5038
Links to Exploration step
ISTEX:42BD07AF7966E59DF1A7C5E2A04236F1F462F8EFLe document en format XML
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Hess</name><affiliation><mods:affiliation>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Clinical Immunology</title><title level="j" type="abbrev">YCLIM</title><idno type="ISSN">1521-6616</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001">2001</date><biblScope unit="volume">100</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="57">57</biblScope><biblScope unit="page" to="70">70</biblScope></imprint><idno type="ISSN">1521-6616</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1521-6616</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>autoaggression</term><term>cyclosporine</term><term>vasculopathy</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Acute phase</term><term>Acute response</term><term>Adoptive</term><term>Adoptive transfer</term><term>Allograft</term><term>Allograft rejection</term><term>Assay</term><term>Atherosclerosis</term><term>Autoaggression</term><term>Autoimmune</term><term>Autoimmune recognition</term><term>Autoimmune vasculopathy</term><term>Autologous</term><term>Autoreactive</term><term>Bone marrow transplant</term><term>Cdr3</term><term>Cdr3 size</term><term>Cell repertoire</term><term>Chloroquine</term><term>Chloroquine treatment</term><term>Chronic allograft rejection</term><term>Chronic gvhd</term><term>Chronic phases</term><term>Chronic rejection</term><term>Chronic sgvhd</term><term>Clonal</term><term>Clonal expansion model</term><term>Control template</term><term>Control template signals</term><term>Cyclosporine</term><term>Cytokine</term><term>Cytokine mrna transcripts</term><term>Determinant</term><term>Effector</term><term>Effector spleen cells</term><term>Endothelial</term><term>Endothelial cells</term><term>Endothelialitis</term><term>Endothelium</term><term>Graft</term><term>Graft atherosclerosis</term><term>Graft vasculopathy</term><term>Grafted</term><term>Grafted heart</term><term>Grafted hearts</term><term>Grafted tissue</term><term>Growth factor beta</term><term>Gvhd</term><term>Heart graft</term><term>Heart grafts</term><term>Heart transplantation</term><term>Hess</term><term>Immunol</term><term>Initial onset</term><term>Invariant chain</term><term>Lesion</term><term>Lymphocyte</term><term>Major histocompatibility</term><term>Medial</term><term>Medial wall</term><term>Mrna</term><term>Mrna transcripts</term><term>Neointima</term><term>Neointima formation</term><term>Nontransplanted</term><term>Nontransplanted heart</term><term>Normal mouse serum</term><term>Prebleed rabbit</term><term>Present studies</term><term>Recent studies</term><term>Receptor</term><term>Sgvhd</term><term>Sgvhd effector</term><term>Sgvhd effector lymphocytes</term><term>Subset</term><term>Syngeneic</term><term>Syngeneic disease</term><term>Syngeneic heart graft</term><term>Syngeneic heart grafts</term><term>Syngeneic heart transplantation</term><term>Target antigen</term><term>Target cells</term><term>Transplant</term><term>Transplantation</term><term>Upregulation</term><term>Vascular</term><term>Vascular disease</term><term>Vascular endothelium</term><term>Vascular lesions</term><term>Vasculopathy</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The use of the immunosuppressive drug cyclosporine A (CsA) in solid organ transplantation can be associated with the development of vasculopathy as part of the complex immune response involved in chronic rejection, including autoimmune recognition. Although CsA can directly affect endothelial cells, this drug alters the T cell repertoire promoting autoimmune recognition. The present studies evaluated the ability of CsA-induced autoreactive T cells to mediate vascular lesions in syngeneic heart grafts. Graft vasculopathy developed in syngeneic heart grafts following either the primary induction of autoimmunity with CsA or the adoptive transfer of CsA-induced autoreactive T cells. Initially, an inflammatory response occurred in the medial wall of the small arterial vessels, accompanied by a perivascular lymphocytic infiltrate (including a lymphocytic infiltrate into the myocardium), followed by progression of vascular disease with endothelial cell proliferation. The development and progression of vascular disease correlated with the cytokine profile of the infiltrating lymphocytes with type 1 cytokines detected early and type 2 cytokines detected as the disease progressed. Initiation of this response correlated with upregulation of the target antigen recognized by the CsA-induced autoreactive T cells, the MHC class II–invariant chain peptide complex. This antigen complex, when upregulated on endothelial cells by interferon, allowed effective targeting by the autoreactive T lymphocytes. Strategies to inhibit the upregulation of MHC class II antigens by treatment of the recipients with chloroquine truncated the disease process. The results of these studies suggest that CsA-induced autoreactive mechanisms can contribute to the development of graft vasculopathy.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>cytokine</json:string><json:string>syngeneic</json:string><json:string>sgvhd</json:string><json:string>lymphocyte</json:string><json:string>transplantation</json:string><json:string>effector</json:string><json:string>graft</json:string><json:string>vascular lesions</json:string><json:string>autoreactive</json:string><json:string>grafted</json:string><json:string>vasculopathy</json:string><json:string>autologous</json:string><json:string>allograft</json:string><json:string>mrna</json:string><json:string>atherosclerosis</json:string><json:string>medial</json:string><json:string>syngeneic heart grafts</json:string><json:string>sgvhd effector</json:string><json:string>adoptive</json:string><json:string>adoptive transfer</json:string><json:string>immunol</json:string><json:string>nontransplanted</json:string><json:string>graft vasculopathy</json:string><json:string>gvhd</json:string><json:string>cdr3</json:string><json:string>receptor</json:string><json:string>autoimmune</json:string><json:string>lesion</json:string><json:string>chloroquine</json:string><json:string>graft atherosclerosis</json:string><json:string>vascular</json:string><json:string>chronic rejection</json:string><json:string>cyclosporine</json:string><json:string>endothelium</json:string><json:string>autoaggression</json:string><json:string>clonal</json:string><json:string>mrna transcripts</json:string><json:string>endothelial cells</json:string><json:string>endothelial</json:string><json:string>hess</json:string><json:string>endothelialitis</json:string><json:string>upregulation</json:string><json:string>neointima</json:string><json:string>subset</json:string><json:string>target cells</json:string><json:string>autoimmune vasculopathy</json:string><json:string>grafted tissue</json:string><json:string>syngeneic disease</json:string><json:string>vascular disease</json:string><json:string>medial wall</json:string><json:string>heart transplantation</json:string><json:string>grafted heart</json:string><json:string>chronic gvhd</json:string><json:string>neointima formation</json:string><json:string>acute response</json:string><json:string>vascular endothelium</json:string><json:string>present studies</json:string><json:string>cytokine mrna transcripts</json:string><json:string>heart grafts</json:string><json:string>nontransplanted heart</json:string><json:string>assay</json:string><json:string>determinant</json:string><json:string>cdr3 size</json:string><json:string>control template</json:string><json:string>clonal expansion model</json:string><json:string>autoimmune recognition</json:string><json:string>grafted hearts</json:string><json:string>acute phase</json:string><json:string>heart graft</json:string><json:string>syngeneic heart graft</json:string><json:string>recent studies</json:string><json:string>transplant</json:string><json:string>invariant chain</json:string><json:string>chronic sgvhd</json:string><json:string>chronic phases</json:string><json:string>cell repertoire</json:string><json:string>initial onset</json:string><json:string>prebleed rabbit</json:string><json:string>normal mouse serum</json:string><json:string>sgvhd effector lymphocytes</json:string><json:string>control template signals</json:string><json:string>target antigen</json:string><json:string>chloroquine treatment</json:string><json:string>syngeneic heart transplantation</json:string><json:string>chronic allograft rejection</json:string><json:string>effector spleen cells</json:string><json:string>allograft rejection</json:string><json:string>major histocompatibility</json:string><json:string>growth factor beta</json:string><json:string>bone marrow transplant</json:string></teeft></keywords><author><json:item><name>Weiran Chen</name><affiliations><json:string>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</json:string></affiliations></json:item><json:item><name>Christopher J. Thoburn</name><affiliations><json:string>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</json:string></affiliations></json:item><json:item><name>Yuji Miura</name><affiliations><json:string>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</json:string></affiliations></json:item><json:item><name>Matthias Sommer</name><affiliations><json:string>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</json:string></affiliations></json:item><json:item><name>Ralph Hruban</name><affiliations><json:string>Department of Pathology, The Johns Hopkins University, Baltimore, Maryland, 21231</json:string></affiliations></json:item><json:item><name>Zhiping Qian</name><affiliations><json:string>Department of Pathology, The Johns Hopkins University, Baltimore, Maryland, 21231</json:string></affiliations></json:item><json:item><name>William Baldwin</name><affiliations><json:string>Department of Pathology, The Johns Hopkins University, Baltimore, Maryland, 21231</json:string></affiliations></json:item><json:item><name>Allan D. Hess</name><affiliations><json:string>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>cyclosporine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>autoaggression</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>vasculopathy</value></json:item></subject><arkIstex>ark:/67375/6H6-SW245SRF-C</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: The use of the immunosuppressive drug cyclosporine A (CsA) in solid organ transplantation can be associated with the development of vasculopathy as part of the complex immune response involved in chronic rejection, including autoimmune recognition. Although CsA can directly affect endothelial cells, this drug alters the T cell repertoire promoting autoimmune recognition. The present studies evaluated the ability of CsA-induced autoreactive T cells to mediate vascular lesions in syngeneic heart grafts. Graft vasculopathy developed in syngeneic heart grafts following either the primary induction of autoimmunity with CsA or the adoptive transfer of CsA-induced autoreactive T cells. Initially, an inflammatory response occurred in the medial wall of the small arterial vessels, accompanied by a perivascular lymphocytic infiltrate (including a lymphocytic infiltrate into the myocardium), followed by progression of vascular disease with endothelial cell proliferation. The development and progression of vascular disease correlated with the cytokine profile of the infiltrating lymphocytes with type 1 cytokines detected early and type 2 cytokines detected as the disease progressed. Initiation of this response correlated with upregulation of the target antigen recognized by the CsA-induced autoreactive T cells, the MHC class II–invariant chain peptide complex. This antigen complex, when upregulated on endothelial cells by interferon, allowed effective targeting by the autoreactive T lymphocytes. Strategies to inhibit the upregulation of MHC class II antigens by treatment of the recipients with chloroquine truncated the disease process. The results of these studies suggest that CsA-induced autoreactive mechanisms can contribute to the development of graft vasculopathy.</abstract><qualityIndicators><score>9.964</score><pdfWordCount>7964</pdfWordCount><pdfCharCount>50462</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>14</pdfPageCount><pdfPageSize>548 x 727 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>247</abstractWordCount><abstractCharCount>1796</abstractCharCount><keywordCount>3</keywordCount></qualityIndicators><title>Autoimmune-Mediated Vasculopathy</title><pmid><json:string>11414746</json:string></pmid><pii><json:string>S1521-6616(01)95038-7</json:string></pii><genre><json:string>research-article</json:string></genre><host><title>Clinical Immunology</title><language><json:string>unknown</json:string></language><publicationDate>2001</publicationDate><issn><json:string>1521-6616</json:string></issn><pii><json:string>S1521-6616(00)X0038-1</json:string></pii><volume>100</volume><issue>1</issue><pages><first>57</first><last>70</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>2001</json:string></date><geogName></geogName><orgName><json:string>Life Technologies</json:string><json:string>Department of Pathology, The Johns Hopkins University, Baltimore, Maryland</json:string><json:string>Biotech</json:string><json:string>The Johns Hopkins University</json:string><json:string>Charles River Breeding Laboratories, Wilmington</json:string><json:string>Sigma Chemical Co.</json:string><json:string>National Institutes of Health, Bethesda, MD</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>William Baldwin</json:string><json:string>Harlan Bioproducts</json:string><json:string>Matthias Sommer</json:string><json:string>Allan D. 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Press</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</p></availability><date>2001</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note>This work was supported by grants AI 24319, HL 58091, CA 82583, and CA 15396 from the National Institutes of Health, Bethesda, MD.</note><note>Received Dec. 20, 2000</note><note type="content">Section title: Regular Article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Autoimmune-Mediated Vasculopathy</title><author xml:id="author-0000"><persName><forename type="first">Weiran</forename><surname>Chen</surname></persName><affiliation>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Christopher J.</forename><surname>Thoburn</surname></persName><affiliation>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Yuji</forename><surname>Miura</surname></persName><affiliation>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Matthias</forename><surname>Sommer</surname></persName><affiliation>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Ralph</forename><surname>Hruban</surname></persName><affiliation>Department of Pathology, The Johns Hopkins University, Baltimore, Maryland, 21231</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Zhiping</forename><surname>Qian</surname></persName><affiliation>Department of Pathology, The Johns Hopkins University, Baltimore, Maryland, 21231</affiliation></author><author xml:id="author-0006"><persName><forename type="first">William</forename><surname>Baldwin</surname></persName><affiliation>Department of Pathology, The Johns Hopkins University, Baltimore, Maryland, 21231</affiliation></author><author xml:id="author-0007"><persName><forename type="first">Allan D.</forename><surname>Hess</surname></persName><affiliation>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</affiliation></author><idno type="istex">42BD07AF7966E59DF1A7C5E2A04236F1F462F8EF</idno><idno type="ark">ark:/67375/6H6-SW245SRF-C</idno><idno type="DOI">10.1006/clim.2001.5038</idno><idno type="PII">S1521-6616(01)95038-7</idno></analytic><monogr><title level="j">Clinical Immunology</title><title level="j" type="abbrev">YCLIM</title><idno type="pISSN">1521-6616</idno><idno type="PII">S1521-6616(00)X0038-1</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001"></date><biblScope unit="volume">100</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="57">57</biblScope><biblScope unit="page" to="70">70</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: The use of the immunosuppressive drug cyclosporine A (CsA) in solid organ transplantation can be associated with the development of vasculopathy as part of the complex immune response involved in chronic rejection, including autoimmune recognition. Although CsA can directly affect endothelial cells, this drug alters the T cell repertoire promoting autoimmune recognition. The present studies evaluated the ability of CsA-induced autoreactive T cells to mediate vascular lesions in syngeneic heart grafts. Graft vasculopathy developed in syngeneic heart grafts following either the primary induction of autoimmunity with CsA or the adoptive transfer of CsA-induced autoreactive T cells. Initially, an inflammatory response occurred in the medial wall of the small arterial vessels, accompanied by a perivascular lymphocytic infiltrate (including a lymphocytic infiltrate into the myocardium), followed by progression of vascular disease with endothelial cell proliferation. The development and progression of vascular disease correlated with the cytokine profile of the infiltrating lymphocytes with type 1 cytokines detected early and type 2 cytokines detected as the disease progressed. Initiation of this response correlated with upregulation of the target antigen recognized by the CsA-induced autoreactive T cells, the MHC class II–invariant chain peptide complex. This antigen complex, when upregulated on endothelial cells by interferon, allowed effective targeting by the autoreactive T lymphocytes. Strategies to inhibit the upregulation of MHC class II antigens by treatment of the recipients with chloroquine truncated the disease process. The results of these studies suggest that CsA-induced autoreactive mechanisms can contribute to the development of graft vasculopathy.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>cyclosporine</term></item><item><term>autoaggression</term></item><item><term>vasculopathy</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2001">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-SW245SRF-C/fulltext.txt</uri></json:item></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" xml:lang="en"><item-info><jid>YCLIM</jid><aid>95038</aid><ce:pii>S1521-6616(01)95038-7</ce:pii><ce:doi>10.1006/clim.2001.5038</ce:doi><ce:copyright type="full-transfer" year="2001">Academic Press</ce:copyright></item-info><head><ce:article-footnote><ce:label>☆</ce:label><ce:note-para>This work was supported by grants AI 24319, HL 58091, CA 82583, and CA 15396 from the National Institutes of Health, Bethesda, MD.</ce:note-para></ce:article-footnote><ce:dochead><ce:textfn>Regular Article</ce:textfn></ce:dochead><ce:title>Autoimmune-Mediated Vasculopathy</ce:title><ce:author-group><ce:author><ce:given-name>Weiran</ce:given-name><ce:surname>Chen</ce:surname><ce:cross-ref refid="A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Christopher J.</ce:given-name><ce:surname>Thoburn</ce:surname><ce:cross-ref refid="A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Yuji</ce:given-name><ce:surname>Miura</ce:surname><ce:cross-ref refid="A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Matthias</ce:given-name><ce:surname>Sommer</ce:surname><ce:cross-ref refid="A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Ralph</ce:given-name><ce:surname>Hruban</ce:surname><ce:cross-ref refid="A2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Zhiping</ce:given-name><ce:surname>Qian</ce:surname><ce:cross-ref refid="A2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>William</ce:given-name><ce:surname>Baldwin</ce:surname><ce:cross-ref refid="A2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Allan D.</ce:given-name><ce:surname>Hess</ce:surname><ce:cross-ref refid="A1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="A2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="A1"><ce:label>a</ce:label><ce:textfn>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</ce:textfn></ce:affiliation><ce:affiliation id="A2"><ce:label>b</ce:label><ce:textfn>Department of Pathology, The Johns Hopkins University, Baltimore, Maryland, 21231</ce:textfn></ce:affiliation></ce:author-group><ce:date-accepted day="28" month="3" year="2001"></ce:date-accepted><ce:miscellaneous>Received Dec. 20, 2000</ce:miscellaneous><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>The use of the immunosuppressive drug cyclosporine A (CsA) in solid organ transplantation can be associated with the development of vasculopathy as part of the complex immune response involved in chronic rejection, including autoimmune recognition. Although CsA can directly affect endothelial cells, this drug alters the T cell repertoire promoting autoimmune recognition. The present studies evaluated the ability of CsA-induced autoreactive T cells to mediate vascular lesions in syngeneic heart grafts. Graft vasculopathy developed in syngeneic heart grafts following either the primary induction of autoimmunity with CsA or the adoptive transfer of CsA-induced autoreactive T cells. Initially, an inflammatory response occurred in the medial wall of the small arterial vessels, accompanied by a perivascular lymphocytic infiltrate (including a lymphocytic infiltrate into the myocardium), followed by progression of vascular disease with endothelial cell proliferation. The development and progression of vascular disease correlated with the cytokine profile of the infiltrating lymphocytes with type 1 cytokines detected early and type 2 cytokines detected as the disease progressed. Initiation of this response correlated with upregulation of the target antigen recognized by the CsA-induced autoreactive T cells, the MHC class II–invariant chain peptide complex. This antigen complex, when upregulated on endothelial cells by interferon, allowed effective targeting by the autoreactive T lymphocytes. Strategies to inhibit the upregulation of MHC class II antigens by treatment of the recipients with chloroquine truncated the disease process. The results of these studies suggest that CsA-induced autoreactive mechanisms can contribute to the development of graft vasculopathy.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>cyclosporine</ce:text></ce:keyword><ce:keyword><ce:text>autoaggression</ce:text></ce:keyword><ce:keyword><ce:text>vasculopathy</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Autoimmune-Mediated Vasculopathy</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Autoimmune-Mediated Vasculopathy</title></titleInfo><name type="personal"><namePart type="given">Weiran</namePart><namePart type="family">Chen</namePart><affiliation>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christopher J.</namePart><namePart type="family">Thoburn</namePart><affiliation>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yuji</namePart><namePart type="family">Miura</namePart><affiliation>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Matthias</namePart><namePart type="family">Sommer</namePart><affiliation>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ralph</namePart><namePart type="family">Hruban</namePart><affiliation>Department of Pathology, The Johns Hopkins University, Baltimore, Maryland, 21231</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Zhiping</namePart><namePart type="family">Qian</namePart><affiliation>Department of Pathology, The Johns Hopkins University, Baltimore, Maryland, 21231</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">William</namePart><namePart type="family">Baldwin</namePart><affiliation>Department of Pathology, The Johns Hopkins University, Baltimore, Maryland, 21231</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Allan D.</namePart><namePart type="family">Hess</namePart><affiliation>Department of Oncology, The Johns Hopkins University, Baltimore, Maryland, 21231</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2001</dateIssued><copyrightDate encoding="w3cdtf">2001</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: The use of the immunosuppressive drug cyclosporine A (CsA) in solid organ transplantation can be associated with the development of vasculopathy as part of the complex immune response involved in chronic rejection, including autoimmune recognition. Although CsA can directly affect endothelial cells, this drug alters the T cell repertoire promoting autoimmune recognition. The present studies evaluated the ability of CsA-induced autoreactive T cells to mediate vascular lesions in syngeneic heart grafts. Graft vasculopathy developed in syngeneic heart grafts following either the primary induction of autoimmunity with CsA or the adoptive transfer of CsA-induced autoreactive T cells. Initially, an inflammatory response occurred in the medial wall of the small arterial vessels, accompanied by a perivascular lymphocytic infiltrate (including a lymphocytic infiltrate into the myocardium), followed by progression of vascular disease with endothelial cell proliferation. The development and progression of vascular disease correlated with the cytokine profile of the infiltrating lymphocytes with type 1 cytokines detected early and type 2 cytokines detected as the disease progressed. Initiation of this response correlated with upregulation of the target antigen recognized by the CsA-induced autoreactive T cells, the MHC class II–invariant chain peptide complex. This antigen complex, when upregulated on endothelial cells by interferon, allowed effective targeting by the autoreactive T lymphocytes. Strategies to inhibit the upregulation of MHC class II antigens by treatment of the recipients with chloroquine truncated the disease process. The results of these studies suggest that CsA-induced autoreactive mechanisms can contribute to the development of graft vasculopathy.</abstract><note>This work was supported by grants AI 24319, HL 58091, CA 82583, and CA 15396 from the National Institutes of Health, Bethesda, MD.</note><note>Received Dec. 20, 2000</note><note type="content">Section title: Regular Article</note><subject lang="en"><genre>Keywords</genre><topic>cyclosporine</topic><topic>autoaggression</topic><topic>vasculopathy</topic></subject><relatedItem type="host"><titleInfo><title>Clinical Immunology</title></titleInfo><titleInfo type="abbreviated"><title>YCLIM</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2001</dateIssued></originInfo><identifier type="ISSN">1521-6616</identifier><identifier type="PII">S1521-6616(00)X0038-1</identifier><part><date>2001</date><detail type="volume"><number>100</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue-pages"><start>1</start><end>127</end></extent><extent unit="pages"><start>57</start><end>70</end></extent></part></relatedItem><identifier type="istex">42BD07AF7966E59DF1A7C5E2A04236F1F462F8EF</identifier><identifier type="ark">ark:/67375/6H6-SW245SRF-C</identifier><identifier type="DOI">10.1006/clim.2001.5038</identifier><identifier type="PII">S1521-6616(01)95038-7</identifier><accessCondition type="use and reproduction" contentType="copyright">©2001 Academic Press</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource><recordOrigin>Academic Press, ©2001</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-SW245SRF-C/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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