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ATG‐Induced Accelerated Immune Senescence: Clinical Implications in Renal Transplant Recipients
Persistent ATG‐induced CD4+ T cell lymphopenia is associated with serious clinical complications. We tested the hypothesis that ATG induces accelerated immune senescence in renal transplant recipients (RTR). Immune senescence biomarkers were analyzed at transplant and one‐year later in 97 incident R...
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| Published in: | American journal of transplantation 2015-04, Vol.15 (4), p.1028-1038 |
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| container_title | American journal of transplantation |
| container_volume | 15 |
| creator | Crepin, T. Carron, C. Roubiou, C. Gaugler, B. Gaiffe, E. Simula‐Faivre, D. Ferrand, C. Tiberghien, P. Chalopin, J.‐M. Moulin, B. Frimat, L. Rieu, P. Saas, P. Ducloux, D. Bamoulid, J. |
| description | Persistent ATG‐induced CD4+ T cell lymphopenia is associated with serious clinical complications. We tested the hypothesis that ATG induces accelerated immune senescence in renal transplant recipients (RTR). Immune senescence biomarkers were analyzed at transplant and one‐year later in 97 incident RTR −62 patients receiving ATG and 35 receiving anti‐CD25 mAb (α‐CD25). This consisted in: (i) thymic output; (ii) bone marrow renewal of CD34+ hematopoietic progenitor cells (CD34+HPC) and lymphoid (l‐HPC) and myeloid (m‐HPC) progenitor ratio; (iii) T cell phenotype; and (iv) measurement of T cell relative telomere length (RTL) and telomerase activity (RTA). Clinical correlates were analyzed with a 3 year follow‐up. Thymic output significantly decreased one‐year posttransplant in ATG‐treated patients. ATG was associated with a significant decrease in l‐HPC/m‐HPC ratio. Late stage differentiated CD57+/CD28− T cells increased in ATG‐treated patients. One‐year posttransplant T cell RTL and RTA were consequently lower in ATG‐treated patients. ATG is associated with accelerated immune senescence. Increased frequency of late differentiated CD4+ T cell frequency at transplantation tended to be predictive of a higher risk of subsequent opportunistic infections and of acute rejection only in ATG‐treated patients but this needs confirmation. Considering pretransplant immune profile may help to select those patients who may benefit from ATG to prevent severe infections and acute rejection.
Analysis of immune senescence biomarkers at transplant and one year later in renal transplant recipients reveals that ATG is not only associated with accelerated immune senescence, but that increased frequency of late differentiated CD4+ T cells at transplantation in ATG‐treated patients tends to be predictive of a higher risk of subsequent opportunistic infections and acute rejection. |
| doi_str_mv | 10.1111/ajt.13092 |
| format | article |
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Analysis of immune senescence biomarkers at transplant and one year later in renal transplant recipients reveals that ATG is not only associated with accelerated immune senescence, but that increased frequency of late differentiated CD4+ T cells at transplantation in ATG‐treated patients tends to be predictive of a higher risk of subsequent opportunistic infections and acute rejection.</description><identifier>ISSN: 1600-6135</identifier><identifier>EISSN: 1600-6143</identifier><identifier>DOI: 10.1111/ajt.13092</identifier><identifier>PMID: 25758660</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Adult ; Antilymphocyte Serum - immunology ; Biomarkers ; Cats ; cell death: senescence ; complication ; Female ; Health risk assessment ; Humans ; immune deficiency ; immunosuppressant ; immunosuppressive regimens ; induction ; Infections ; Kidney Transplantation ; Lymphocytes ; Male ; Middle Aged ; polyclonal preparations: rabbit antithymocyte globulin ; Senescence ; T-Lymphocytes - immunology ; Transplants & implants</subject><ispartof>American journal of transplantation, 2015-04, Vol.15 (4), p.1028-1038</ispartof><rights>Copyright 2015 The American Society of Transplantation and the American Society of Transplant Surgeons</rights><rights>Copyright 2015 The American Society of Transplantation and the American Society of Transplant Surgeons.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fajt.13092$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fajt.13092$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,786,790,27957,27958,50923,51032</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25758660$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Crepin, T.</creatorcontrib><creatorcontrib>Carron, C.</creatorcontrib><creatorcontrib>Roubiou, C.</creatorcontrib><creatorcontrib>Gaugler, B.</creatorcontrib><creatorcontrib>Gaiffe, E.</creatorcontrib><creatorcontrib>Simula‐Faivre, D.</creatorcontrib><creatorcontrib>Ferrand, C.</creatorcontrib><creatorcontrib>Tiberghien, P.</creatorcontrib><creatorcontrib>Chalopin, J.‐M.</creatorcontrib><creatorcontrib>Moulin, B.</creatorcontrib><creatorcontrib>Frimat, L.</creatorcontrib><creatorcontrib>Rieu, P.</creatorcontrib><creatorcontrib>Saas, P.</creatorcontrib><creatorcontrib>Ducloux, D.</creatorcontrib><creatorcontrib>Bamoulid, J.</creatorcontrib><title>ATG‐Induced Accelerated Immune Senescence: Clinical Implications in Renal Transplant Recipients</title><title>American journal of transplantation</title><addtitle>Am J Transplant</addtitle><description>Persistent ATG‐induced CD4+ T cell lymphopenia is associated with serious clinical complications. We tested the hypothesis that ATG induces accelerated immune senescence in renal transplant recipients (RTR). Immune senescence biomarkers were analyzed at transplant and one‐year later in 97 incident RTR −62 patients receiving ATG and 35 receiving anti‐CD25 mAb (α‐CD25). This consisted in: (i) thymic output; (ii) bone marrow renewal of CD34+ hematopoietic progenitor cells (CD34+HPC) and lymphoid (l‐HPC) and myeloid (m‐HPC) progenitor ratio; (iii) T cell phenotype; and (iv) measurement of T cell relative telomere length (RTL) and telomerase activity (RTA). Clinical correlates were analyzed with a 3 year follow‐up. Thymic output significantly decreased one‐year posttransplant in ATG‐treated patients. ATG was associated with a significant decrease in l‐HPC/m‐HPC ratio. Late stage differentiated CD57+/CD28− T cells increased in ATG‐treated patients. One‐year posttransplant T cell RTL and RTA were consequently lower in ATG‐treated patients. ATG is associated with accelerated immune senescence. Increased frequency of late differentiated CD4+ T cell frequency at transplantation tended to be predictive of a higher risk of subsequent opportunistic infections and of acute rejection only in ATG‐treated patients but this needs confirmation. Considering pretransplant immune profile may help to select those patients who may benefit from ATG to prevent severe infections and acute rejection.
Analysis of immune senescence biomarkers at transplant and one year later in renal transplant recipients reveals that ATG is not only associated with accelerated immune senescence, but that increased frequency of late differentiated CD4+ T cells at transplantation in ATG‐treated patients tends to be predictive of a higher risk of subsequent opportunistic infections and acute rejection.</description><subject>Adult</subject><subject>Antilymphocyte Serum - immunology</subject><subject>Biomarkers</subject><subject>Cats</subject><subject>cell death: senescence</subject><subject>complication</subject><subject>Female</subject><subject>Health risk assessment</subject><subject>Humans</subject><subject>immune deficiency</subject><subject>immunosuppressant</subject><subject>immunosuppressive regimens</subject><subject>induction</subject><subject>Infections</subject><subject>Kidney Transplantation</subject><subject>Lymphocytes</subject><subject>Male</subject><subject>Middle Aged</subject><subject>polyclonal preparations: rabbit antithymocyte globulin</subject><subject>Senescence</subject><subject>T-Lymphocytes - immunology</subject><subject>Transplants & implants</subject><issn>1600-6135</issn><issn>1600-6143</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNpdkU1OwzAQhS0EolBYcAEUiQ2btLYT_4RdVUEpqoQEYR05zkRylTghToS64wickZNg2tIFs_HTm0-jGT-ErgieEF9Tte4nJMIJPUJnhGMcchJHxwcdsRE6d26NMRFU0lM0okwwyTk-Q2qWLr4_v5a2GDQUwUxrqKBTvdfLuh4sBK9gwWmwGu6CeWWs0aryvbbyojeNdYGxwQtY76adsq6tlO29oU1rwPbuAp2UqnJwuX_H6O3hPp0_hqvnxXI-W4UtFQkNaZLneawFziUtmZZMqwiiUsWJknkRgwJWKG9IgRUvclaIHCeYMqkYlZKU0Rjd7ua2XfM-gOuz2vi9K78ONIPLCOdcUME49-jNP3TdDJ2_YEvFLJEJFZ663lNDXkORtZ2pVbfJ_j7PA9Md8GEq2Bz6BGe_qWQ-lWybSjZ7Srci-gFzBH-o</recordid><startdate>201504</startdate><enddate>201504</enddate><creator>Crepin, T.</creator><creator>Carron, C.</creator><creator>Roubiou, C.</creator><creator>Gaugler, B.</creator><creator>Gaiffe, E.</creator><creator>Simula‐Faivre, D.</creator><creator>Ferrand, C.</creator><creator>Tiberghien, P.</creator><creator>Chalopin, J.‐M.</creator><creator>Moulin, B.</creator><creator>Frimat, L.</creator><creator>Rieu, P.</creator><creator>Saas, P.</creator><creator>Ducloux, D.</creator><creator>Bamoulid, J.</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QP</scope><scope>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201504</creationdate><title>ATG‐Induced Accelerated Immune Senescence: Clinical Implications in Renal Transplant Recipients</title><author>Crepin, T. ; Carron, C. ; Roubiou, C. ; Gaugler, B. ; Gaiffe, E. ; Simula‐Faivre, D. ; Ferrand, C. ; Tiberghien, P. ; Chalopin, J.‐M. ; Moulin, B. ; Frimat, L. ; Rieu, P. ; Saas, P. ; Ducloux, D. ; Bamoulid, J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p2792-29bbb4c70b82f5c85ca3e3fa49a8bd4eae5dae3f870a6db5d7b090258a52881f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adult</topic><topic>Antilymphocyte Serum - immunology</topic><topic>Biomarkers</topic><topic>Cats</topic><topic>cell death: senescence</topic><topic>complication</topic><topic>Female</topic><topic>Health risk assessment</topic><topic>Humans</topic><topic>immune deficiency</topic><topic>immunosuppressant</topic><topic>immunosuppressive regimens</topic><topic>induction</topic><topic>Infections</topic><topic>Kidney Transplantation</topic><topic>Lymphocytes</topic><topic>Male</topic><topic>Middle Aged</topic><topic>polyclonal preparations: rabbit antithymocyte globulin</topic><topic>Senescence</topic><topic>T-Lymphocytes - immunology</topic><topic>Transplants & implants</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Crepin, T.</creatorcontrib><creatorcontrib>Carron, C.</creatorcontrib><creatorcontrib>Roubiou, C.</creatorcontrib><creatorcontrib>Gaugler, B.</creatorcontrib><creatorcontrib>Gaiffe, E.</creatorcontrib><creatorcontrib>Simula‐Faivre, D.</creatorcontrib><creatorcontrib>Ferrand, C.</creatorcontrib><creatorcontrib>Tiberghien, P.</creatorcontrib><creatorcontrib>Chalopin, J.‐M.</creatorcontrib><creatorcontrib>Moulin, B.</creatorcontrib><creatorcontrib>Frimat, L.</creatorcontrib><creatorcontrib>Rieu, P.</creatorcontrib><creatorcontrib>Saas, P.</creatorcontrib><creatorcontrib>Ducloux, D.</creatorcontrib><creatorcontrib>Bamoulid, J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Crepin, T.</au><au>Carron, C.</au><au>Roubiou, C.</au><au>Gaugler, B.</au><au>Gaiffe, E.</au><au>Simula‐Faivre, D.</au><au>Ferrand, C.</au><au>Tiberghien, P.</au><au>Chalopin, J.‐M.</au><au>Moulin, B.</au><au>Frimat, L.</au><au>Rieu, P.</au><au>Saas, P.</au><au>Ducloux, D.</au><au>Bamoulid, J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ATG‐Induced Accelerated Immune Senescence: Clinical Implications in Renal Transplant Recipients</atitle><jtitle>American journal of transplantation</jtitle><addtitle>Am J Transplant</addtitle><date>2015-04</date><risdate>2015</risdate><volume>15</volume><issue>4</issue><spage>1028</spage><epage>1038</epage><pages>1028-1038</pages><issn>1600-6135</issn><eissn>1600-6143</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Persistent ATG‐induced CD4+ T cell lymphopenia is associated with serious clinical complications. We tested the hypothesis that ATG induces accelerated immune senescence in renal transplant recipients (RTR). Immune senescence biomarkers were analyzed at transplant and one‐year later in 97 incident RTR −62 patients receiving ATG and 35 receiving anti‐CD25 mAb (α‐CD25). This consisted in: (i) thymic output; (ii) bone marrow renewal of CD34+ hematopoietic progenitor cells (CD34+HPC) and lymphoid (l‐HPC) and myeloid (m‐HPC) progenitor ratio; (iii) T cell phenotype; and (iv) measurement of T cell relative telomere length (RTL) and telomerase activity (RTA). Clinical correlates were analyzed with a 3 year follow‐up. Thymic output significantly decreased one‐year posttransplant in ATG‐treated patients. ATG was associated with a significant decrease in l‐HPC/m‐HPC ratio. Late stage differentiated CD57+/CD28− T cells increased in ATG‐treated patients. One‐year posttransplant T cell RTL and RTA were consequently lower in ATG‐treated patients. ATG is associated with accelerated immune senescence. Increased frequency of late differentiated CD4+ T cell frequency at transplantation tended to be predictive of a higher risk of subsequent opportunistic infections and of acute rejection only in ATG‐treated patients but this needs confirmation. Considering pretransplant immune profile may help to select those patients who may benefit from ATG to prevent severe infections and acute rejection.
Analysis of immune senescence biomarkers at transplant and one year later in renal transplant recipients reveals that ATG is not only associated with accelerated immune senescence, but that increased frequency of late differentiated CD4+ T cells at transplantation in ATG‐treated patients tends to be predictive of a higher risk of subsequent opportunistic infections and acute rejection.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>25758660</pmid><doi>10.1111/ajt.13092</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Antilymphocyte Serum - immunology Biomarkers Cats cell death: senescence complication Female Health risk assessment Humans immune deficiency immunosuppressant immunosuppressive regimens induction Infections Kidney Transplantation Lymphocytes Male Middle Aged polyclonal preparations: rabbit antithymocyte globulin Senescence T-Lymphocytes - immunology Transplants & implants |
| title | ATG‐Induced Accelerated Immune Senescence: Clinical Implications in Renal Transplant Recipients |
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