The role of the graft endothelium in transplant rejection: Evidence that endothelial activation may serve as a clinical marker for the development of chronic rejection
: In this review, we discuss the role of the allograft endothelium in the recruitment and activation of leukocytes during acute and chronic rejection. We discuss associations among endothelial activation responses, the expression of adhesion molecules, chemokines and chemokine receptors, and rejecti...
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Veröffentlicht in: | Pediatric transplantation 2000-11, Vol.4 (4), p.252-260 |
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container_title | Pediatric transplantation |
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creator | Denton, Mark D. Davis, Stacy F. Baum, Michelle A. Melter, Michael Reinders, Marlies E. J. Exeni, Andrea Samsonov, Dmitry V. Fang, Jim Ganz, Peter Briscoe, David M. |
description | : In this review, we discuss the role of the allograft endothelium in the recruitment and activation of leukocytes during acute and chronic rejection. We discuss associations among endothelial activation responses, the expression of adhesion molecules, chemokines and chemokine receptors, and rejection; and we propose that endothelial vascular cellular adhesion molecule‐1 (VCAM‐1) may be used as a surrogate marker of acute rejection and allograft vasculopathy. In addition, we describe potential mechanistic interpretations of persistent endothelial cell (EC) expression of major histocompatibility complex (MHC) class II molecules in allorecognition. The graft endothelium may provide an antigen‐specific signal to transmigrating, previously activated, T cells and may induce B7 expression on locally transmigrating leukocytes to promote costimulation. Taken together, these functions of the EC provide it with a potent regulatory role in rejection and in the maintenance of T‐cell activation via the direct and/or the indirect pathways of allorecognition. |
doi_str_mv | 10.1034/j.1399-3046.2000.00031.x |
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The graft endothelium may provide an antigen‐specific signal to transmigrating, previously activated, T cells and may induce B7 expression on locally transmigrating leukocytes to promote costimulation. Taken together, these functions of the EC provide it with a potent regulatory role in rejection and in the maintenance of T‐cell activation via the direct and/or the indirect pathways of allorecognition.</description><identifier>ISSN: 1397-3142</identifier><identifier>EISSN: 1399-3046</identifier><identifier>DOI: 10.1034/j.1399-3046.2000.00031.x</identifier><identifier>PMID: 11079263</identifier><language>eng</language><publisher>Copenhagen, Denmark: Munksgaard International Publishers</publisher><subject>Biological and medical sciences ; Biomarkers - analysis ; Chronic Disease ; endothelium ; Endothelium, Vascular - immunology ; Graft Rejection - immunology ; Humans ; Medical sciences ; rejection ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the heart ; transplantation ; Transplantation, Homologous ; Vascular Cell Adhesion Molecule-1 - analysis</subject><ispartof>Pediatric transplantation, 2000-11, Vol.4 (4), p.252-260</ispartof><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3471-3587d0eab96b128036e202e6d410202c421c89837fd925f094e5e73e68daa2203</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1034%2Fj.1399-3046.2000.00031.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1034%2Fj.1399-3046.2000.00031.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1515151$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11079263$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Denton, Mark D.</creatorcontrib><creatorcontrib>Davis, Stacy F.</creatorcontrib><creatorcontrib>Baum, Michelle A.</creatorcontrib><creatorcontrib>Melter, Michael</creatorcontrib><creatorcontrib>Reinders, Marlies E. J.</creatorcontrib><creatorcontrib>Exeni, Andrea</creatorcontrib><creatorcontrib>Samsonov, Dmitry V.</creatorcontrib><creatorcontrib>Fang, Jim</creatorcontrib><creatorcontrib>Ganz, Peter</creatorcontrib><creatorcontrib>Briscoe, David M.</creatorcontrib><title>The role of the graft endothelium in transplant rejection: Evidence that endothelial activation may serve as a clinical marker for the development of chronic rejection</title><title>Pediatric transplantation</title><addtitle>Pediatr Transplant</addtitle><description>: In this review, we discuss the role of the allograft endothelium in the recruitment and activation of leukocytes during acute and chronic rejection. We discuss associations among endothelial activation responses, the expression of adhesion molecules, chemokines and chemokine receptors, and rejection; and we propose that endothelial vascular cellular adhesion molecule‐1 (VCAM‐1) may be used as a surrogate marker of acute rejection and allograft vasculopathy. In addition, we describe potential mechanistic interpretations of persistent endothelial cell (EC) expression of major histocompatibility complex (MHC) class II molecules in allorecognition. The graft endothelium may provide an antigen‐specific signal to transmigrating, previously activated, T cells and may induce B7 expression on locally transmigrating leukocytes to promote costimulation. Taken together, these functions of the EC provide it with a potent regulatory role in rejection and in the maintenance of T‐cell activation via the direct and/or the indirect pathways of allorecognition.</description><subject>Biological and medical sciences</subject><subject>Biomarkers - analysis</subject><subject>Chronic Disease</subject><subject>endothelium</subject><subject>Endothelium, Vascular - immunology</subject><subject>Graft Rejection - immunology</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>rejection</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Surgery of the heart</subject><subject>transplantation</subject><subject>Transplantation, Homologous</subject><subject>Vascular Cell Adhesion Molecule-1 - analysis</subject><issn>1397-3142</issn><issn>1399-3046</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkd9u0zAUxiMEYmPwCsgXiLtk_hcnQeKCVWWbNDHEipC4sVznhLkkcbHT0j7RXnMnbbVyiSzLx_Lv8-fjL0kIoxmjQp4vMiaqKhVUqoxTSjOcgmWbZ8np08HzXV2kgkl-kryKcUEpU7KUL5MTxmhRcSVOk4fZPZDgWyC-IQPWv4JpBgJ97XHXulVHXE-GYPq4bE0_kAALsIPz_QcyXbsaeguoM_9ITEsMEmszUqQzWxIhrIGYSAyxreudRaQz4TcE0viws61hDa1fdoAW-BJ7HzxyR7fXyYvGtBHeHNaz5Pvn6Wxyld7cXl5PPt2kVsiCpSIvi5qCmVdqznhJhQJOOahaMoqFlZzZsipF0dQVzxtaScihEKDK2hjOqThL3u_vXQb_ZwVx0J2LFlrsHfwq6oJLltNSIVjuQRt8jAEavQwOm9pqRvUYkl7oMQs9ZqHHkPQuJL1B6duDx2reQX0UHlJB4N0BMBH_qsHfty4euXw3EPu4x_66Frb_7a-_TmffsEJ9ute7OMDmSY_BaFWIItc_vlzqCWd3F5Ld6Z_iEUtBvkk</recordid><startdate>200011</startdate><enddate>200011</enddate><creator>Denton, Mark D.</creator><creator>Davis, Stacy F.</creator><creator>Baum, Michelle A.</creator><creator>Melter, Michael</creator><creator>Reinders, Marlies E. J.</creator><creator>Exeni, Andrea</creator><creator>Samsonov, Dmitry V.</creator><creator>Fang, Jim</creator><creator>Ganz, Peter</creator><creator>Briscoe, David M.</creator><general>Munksgaard International Publishers</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200011</creationdate><title>The role of the graft endothelium in transplant rejection: Evidence that endothelial activation may serve as a clinical marker for the development of chronic rejection</title><author>Denton, Mark D. ; Davis, Stacy F. ; Baum, Michelle A. ; Melter, Michael ; Reinders, Marlies E. J. ; Exeni, Andrea ; Samsonov, Dmitry V. ; Fang, Jim ; Ganz, Peter ; Briscoe, David M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3471-3587d0eab96b128036e202e6d410202c421c89837fd925f094e5e73e68daa2203</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Biological and medical sciences</topic><topic>Biomarkers - analysis</topic><topic>Chronic Disease</topic><topic>endothelium</topic><topic>Endothelium, Vascular - immunology</topic><topic>Graft Rejection - immunology</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>rejection</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Surgery of the heart</topic><topic>transplantation</topic><topic>Transplantation, Homologous</topic><topic>Vascular Cell Adhesion Molecule-1 - analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Denton, Mark D.</creatorcontrib><creatorcontrib>Davis, Stacy F.</creatorcontrib><creatorcontrib>Baum, Michelle A.</creatorcontrib><creatorcontrib>Melter, Michael</creatorcontrib><creatorcontrib>Reinders, Marlies E. J.</creatorcontrib><creatorcontrib>Exeni, Andrea</creatorcontrib><creatorcontrib>Samsonov, Dmitry V.</creatorcontrib><creatorcontrib>Fang, Jim</creatorcontrib><creatorcontrib>Ganz, Peter</creatorcontrib><creatorcontrib>Briscoe, David M.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Pediatric transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Denton, Mark D.</au><au>Davis, Stacy F.</au><au>Baum, Michelle A.</au><au>Melter, Michael</au><au>Reinders, Marlies E. 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We discuss associations among endothelial activation responses, the expression of adhesion molecules, chemokines and chemokine receptors, and rejection; and we propose that endothelial vascular cellular adhesion molecule‐1 (VCAM‐1) may be used as a surrogate marker of acute rejection and allograft vasculopathy. In addition, we describe potential mechanistic interpretations of persistent endothelial cell (EC) expression of major histocompatibility complex (MHC) class II molecules in allorecognition. The graft endothelium may provide an antigen‐specific signal to transmigrating, previously activated, T cells and may induce B7 expression on locally transmigrating leukocytes to promote costimulation. Taken together, these functions of the EC provide it with a potent regulatory role in rejection and in the maintenance of T‐cell activation via the direct and/or the indirect pathways of allorecognition.</abstract><cop>Copenhagen, Denmark</cop><pub>Munksgaard International Publishers</pub><pmid>11079263</pmid><doi>10.1034/j.1399-3046.2000.00031.x</doi><tpages>9</tpages></addata></record> |
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subjects | Biological and medical sciences Biomarkers - analysis Chronic Disease endothelium Endothelium, Vascular - immunology Graft Rejection - immunology Humans Medical sciences rejection Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the heart transplantation Transplantation, Homologous Vascular Cell Adhesion Molecule-1 - analysis |
title | The role of the graft endothelium in transplant rejection: Evidence that endothelial activation may serve as a clinical marker for the development of chronic rejection |
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