Detection of donor-specific hyporesponsiveness following late failure of human renal allografts
Detection of donor-specific hyporesponsiveness following late failure of human renal allografts. Limiting dilution assays to measure the frequency of interleukin-2-secreting peripheral blood T cells were carried out in patients, whose renal allografts had failed due to acute rejection (9 patients) a...
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| Veröffentlicht in: | Kidney international 1996-09, Vol.50 (3), p.1019-1025 |
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| creator | Mason, Philip D. Robinson, Catherine M. Lechler, Robert I. |
| description | Detection of donor-specific hyporesponsiveness following late failure of human renal allografts. Limiting dilution assays to measure the frequency of interleukin-2-secreting peripheral blood T cells were carried out in patients, whose renal allografts had failed due to acute rejection (9 patients) and in patients whose grafts failed more than two years after transplantation without any recent evidence of acute rejection. Using a modified form of the assay we demonstrate that nearly half of 18 patients whose renal transplants had failed after more than two years have low or undetectable HTLp frequencies against donor, but not third-party DR antigens. No such difference was observed in any of the nine patients studied whose transplants were lost from early acute rejection. These results provide the first indication that, as in rodent models of transplantation, T cell unresponsiveness towards donor MHC antigens can occur following prolonged residence of an allograft in humans. Furthermore, the results suggest that chronic rejection may be driven by mechanisms other than direct allorecognition. The assay may be a valuable tool to study the evolution of donor-specific direct T cell alloresponsiveness in patients with well-functioning grafts. |
| doi_str_mv | 10.1038/ki.1996.404 |
| format | Article |
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Limiting dilution assays to measure the frequency of interleukin-2-secreting peripheral blood T cells were carried out in patients, whose renal allografts had failed due to acute rejection (9 patients) and in patients whose grafts failed more than two years after transplantation without any recent evidence of acute rejection. Using a modified form of the assay we demonstrate that nearly half of 18 patients whose renal transplants had failed after more than two years have low or undetectable HTLp frequencies against donor, but not third-party DR antigens. No such difference was observed in any of the nine patients studied whose transplants were lost from early acute rejection. These results provide the first indication that, as in rodent models of transplantation, T cell unresponsiveness towards donor MHC antigens can occur following prolonged residence of an allograft in humans. Furthermore, the results suggest that chronic rejection may be driven by mechanisms other than direct allorecognition. The assay may be a valuable tool to study the evolution of donor-specific direct T cell alloresponsiveness in patients with well-functioning grafts.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1038/ki.1996.404</identifier><identifier>PMID: 8872979</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Cell Line - immunology ; Chronic Disease ; Graft Rejection - immunology ; Hematopoietic Stem Cells - cytology ; HLA-DR Antigens - immunology ; Humans ; Indicator Dilution Techniques ; Interleukin-2 - analysis ; Interleukin-2 - metabolism ; Isoantigens ; Kidney Transplantation - immunology ; Lymphocyte Count ; Medical sciences ; Mice ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the urinary system ; T-Lymphocytes - cytology ; Tissue Donors ; Transplantation, Homologous</subject><ispartof>Kidney international, 1996-09, Vol.50 (3), p.1019-1025</ispartof><rights>1996 International Society of Nephrology</rights><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-6e71ca1437166811a8dfae3ea4bdd082e9f69075d961393b87807d0b8f3bd1d53</citedby><cites>FETCH-LOGICAL-c396t-6e71ca1437166811a8dfae3ea4bdd082e9f69075d961393b87807d0b8f3bd1d53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3202351$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8872979$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mason, Philip D.</creatorcontrib><creatorcontrib>Robinson, Catherine M.</creatorcontrib><creatorcontrib>Lechler, Robert I.</creatorcontrib><title>Detection of donor-specific hyporesponsiveness following late failure of human renal allografts</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Detection of donor-specific hyporesponsiveness following late failure of human renal allografts. Limiting dilution assays to measure the frequency of interleukin-2-secreting peripheral blood T cells were carried out in patients, whose renal allografts had failed due to acute rejection (9 patients) and in patients whose grafts failed more than two years after transplantation without any recent evidence of acute rejection. Using a modified form of the assay we demonstrate that nearly half of 18 patients whose renal transplants had failed after more than two years have low or undetectable HTLp frequencies against donor, but not third-party DR antigens. No such difference was observed in any of the nine patients studied whose transplants were lost from early acute rejection. These results provide the first indication that, as in rodent models of transplantation, T cell unresponsiveness towards donor MHC antigens can occur following prolonged residence of an allograft in humans. Furthermore, the results suggest that chronic rejection may be driven by mechanisms other than direct allorecognition. The assay may be a valuable tool to study the evolution of donor-specific direct T cell alloresponsiveness in patients with well-functioning grafts.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Line - immunology</subject><subject>Chronic Disease</subject><subject>Graft Rejection - immunology</subject><subject>Hematopoietic Stem Cells - cytology</subject><subject>HLA-DR Antigens - immunology</subject><subject>Humans</subject><subject>Indicator Dilution Techniques</subject><subject>Interleukin-2 - analysis</subject><subject>Interleukin-2 - metabolism</subject><subject>Isoantigens</subject><subject>Kidney Transplantation - immunology</subject><subject>Lymphocyte Count</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Surgery of the urinary system</subject><subject>T-Lymphocytes - cytology</subject><subject>Tissue Donors</subject><subject>Transplantation, Homologous</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkE2LFDEQhoMo67h68iz0QbxIj0mn00mOsn7Cghc9h3RS2Y2bSdpU98r-ezPMsCdPRfE-9RY8hLxmdM8oVx_u4p5pPe1HOj4hOyYG3jMpxFOyo1SJfhBcPScvEH_TtmtOL8iFUnLQUu-I-QQruDWW3JXQ-ZJL7XEBF0N03e3DUirgUjLGe8iA2IWSUvkb802X7ApdsDFtFY63t9vB5q5CtqmzDbqpNqz4kjwLNiG8Os9L8uvL559X3_rrH1-_X3287h3X09pPIJmzbOSSTZNizCofLHCw4-w9VQPoMGkqhdcT45rPSioqPZ1V4LNnXvBL8u7Uu9TyZwNczSGig5RshrKhkWps5ZQ28P0JdLUgVghmqfFg64Nh1Bx1mrtojjpN09noN-fabT6Af2TP_lr-9pxbdDaFarOL-IjxgQ5csIaJEwZNwX2EatBFyA58rM2-8SX-9_0_iqmQbw</recordid><startdate>19960901</startdate><enddate>19960901</enddate><creator>Mason, Philip D.</creator><creator>Robinson, Catherine M.</creator><creator>Lechler, Robert I.</creator><general>Elsevier Inc</general><general>Nature Publishing</general><scope>6I.</scope><scope>AAFTH</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>19960901</creationdate><title>Detection of donor-specific hyporesponsiveness following late failure of human renal allografts</title><author>Mason, Philip D. ; Robinson, Catherine M. ; Lechler, Robert I.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-6e71ca1437166811a8dfae3ea4bdd082e9f69075d961393b87807d0b8f3bd1d53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Line - immunology</topic><topic>Chronic Disease</topic><topic>Graft Rejection - immunology</topic><topic>Hematopoietic Stem Cells - cytology</topic><topic>HLA-DR Antigens - immunology</topic><topic>Humans</topic><topic>Indicator Dilution Techniques</topic><topic>Interleukin-2 - analysis</topic><topic>Interleukin-2 - metabolism</topic><topic>Isoantigens</topic><topic>Kidney Transplantation - immunology</topic><topic>Lymphocyte Count</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Surgery of the urinary system</topic><topic>T-Lymphocytes - cytology</topic><topic>Tissue Donors</topic><topic>Transplantation, Homologous</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mason, Philip D.</creatorcontrib><creatorcontrib>Robinson, Catherine M.</creatorcontrib><creatorcontrib>Lechler, Robert I.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mason, Philip D.</au><au>Robinson, Catherine M.</au><au>Lechler, Robert I.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Detection of donor-specific hyporesponsiveness following late failure of human renal allografts</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>1996-09-01</date><risdate>1996</risdate><volume>50</volume><issue>3</issue><spage>1019</spage><epage>1025</epage><pages>1019-1025</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Detection of donor-specific hyporesponsiveness following late failure of human renal allografts. Limiting dilution assays to measure the frequency of interleukin-2-secreting peripheral blood T cells were carried out in patients, whose renal allografts had failed due to acute rejection (9 patients) and in patients whose grafts failed more than two years after transplantation without any recent evidence of acute rejection. Using a modified form of the assay we demonstrate that nearly half of 18 patients whose renal transplants had failed after more than two years have low or undetectable HTLp frequencies against donor, but not third-party DR antigens. No such difference was observed in any of the nine patients studied whose transplants were lost from early acute rejection. These results provide the first indication that, as in rodent models of transplantation, T cell unresponsiveness towards donor MHC antigens can occur following prolonged residence of an allograft in humans. Furthermore, the results suggest that chronic rejection may be driven by mechanisms other than direct allorecognition. The assay may be a valuable tool to study the evolution of donor-specific direct T cell alloresponsiveness in patients with well-functioning grafts.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>8872979</pmid><doi>10.1038/ki.1996.404</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Kidney international, 1996-09, Vol.50 (3), p.1019-1025 |
| issn | 0085-2538 1523-1755 |
| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Biological and medical sciences Cell Line - immunology Chronic Disease Graft Rejection - immunology Hematopoietic Stem Cells - cytology HLA-DR Antigens - immunology Humans Indicator Dilution Techniques Interleukin-2 - analysis Interleukin-2 - metabolism Isoantigens Kidney Transplantation - immunology Lymphocyte Count Medical sciences Mice Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the urinary system T-Lymphocytes - cytology Tissue Donors Transplantation, Homologous |
| title | Detection of donor-specific hyporesponsiveness following late failure of human renal allografts |
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