Presence of antibodies against HLA class I and class II molecules in children before and after allo‐HSCT. Alloantibodies before and after HSCT
A severe complication of allogeneic hematopoietic stem cell transplantation (HSCT) is graft failure (GF). Among others, donor‐specific anti‐HLA antibodies (DSA) are associated with graft rejection after allogeneic or haploidentical transplantation in adults. Knowledge of DSA and pediatric recipients...
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Veröffentlicht in: | HLA 2023-01, Vol.101 (1), p.16-23 |
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creator | Morán‐Espinosa, Maricarmen Angeles‐Floriano, Tania Parra‐Ortega, Israel Gaytán‐Morales, Félix Castorena‐Villa, Iván López‐Martínez, Briceida Ortiz‐Navarrete, Vianney Olvera‐Gómez, Irlanda |
description | A severe complication of allogeneic hematopoietic stem cell transplantation (HSCT) is graft failure (GF). Among others, donor‐specific anti‐HLA antibodies (DSA) are associated with graft rejection after allogeneic or haploidentical transplantation in adults. Knowledge of DSA and pediatric recipients is limited. Hence, we aimed to generate more information about the presence of DSA (pre‐ and post‐HSCT) and the clinical outcomes (graft rejection and poor function) in children. We identified DSA in 27% of the patients. We observed a higher frequency (50%) of DSA‐bearing patients with a benign disease diagnosis than those diagnosed with leukemia (16.66%). We observed graft rejection in one patient (with DSA against two alleles of HLA class I molecules) and poor function in three recipients during the first 30 days after HSCT in the absence of DSA. The presence of donor and nondonor HLA‐specific antibodies decreased substantially after transplantation. After the transplant, we identified two patients with DSA specific for HLA class I molecules (independent of clinical relevance), and four recipients showed PGF in the absence of DSA. We were unable to establish any association between the presence of DSA and a clinical outcome: graft failure or prevalence of viral infection. |
doi_str_mv | 10.1111/tan.14817 |
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Alloantibodies before and after HSCT</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Morán‐Espinosa, Maricarmen ; Angeles‐Floriano, Tania ; Parra‐Ortega, Israel ; Gaytán‐Morales, Félix ; Castorena‐Villa, Iván ; López‐Martínez, Briceida ; Ortiz‐Navarrete, Vianney ; Olvera‐Gómez, Irlanda</creator><creatorcontrib>Morán‐Espinosa, Maricarmen ; Angeles‐Floriano, Tania ; Parra‐Ortega, Israel ; Gaytán‐Morales, Félix ; Castorena‐Villa, Iván ; López‐Martínez, Briceida ; Ortiz‐Navarrete, Vianney ; Olvera‐Gómez, Irlanda</creatorcontrib><description>A severe complication of allogeneic hematopoietic stem cell transplantation (HSCT) is graft failure (GF). Among others, donor‐specific anti‐HLA antibodies (DSA) are associated with graft rejection after allogeneic or haploidentical transplantation in adults. Knowledge of DSA and pediatric recipients is limited. Hence, we aimed to generate more information about the presence of DSA (pre‐ and post‐HSCT) and the clinical outcomes (graft rejection and poor function) in children. We identified DSA in 27% of the patients. We observed a higher frequency (50%) of DSA‐bearing patients with a benign disease diagnosis than those diagnosed with leukemia (16.66%). We observed graft rejection in one patient (with DSA against two alleles of HLA class I molecules) and poor function in three recipients during the first 30 days after HSCT in the absence of DSA. The presence of donor and nondonor HLA‐specific antibodies decreased substantially after transplantation. After the transplant, we identified two patients with DSA specific for HLA class I molecules (independent of clinical relevance), and four recipients showed PGF in the absence of DSA. We were unable to establish any association between the presence of DSA and a clinical outcome: graft failure or prevalence of viral infection.</description><identifier>ISSN: 2059-2302</identifier><identifier>EISSN: 2059-2310</identifier><identifier>DOI: 10.1111/tan.14817</identifier><identifier>PMID: 36100956</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Alleles ; alloantibodies ; Child ; graft failure ; Hematopoietic Stem Cell Transplantation ; Histocompatibility Antigens Class I ; Histocompatibility Antigens Class II ; Humans ; Isoantibodies ; poor function ; viral infections</subject><ispartof>HLA, 2023-01, Vol.101 (1), p.16-23</ispartof><rights>2022 John Wiley & Sons Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c2157-15e34c813f697f04930a945fb4bd00579c751746051b91e2d49d312ca4270a213</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Ftan.14817$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Ftan.14817$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,778,782,1414,27913,27914,45563,45564</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36100956$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Morán‐Espinosa, Maricarmen</creatorcontrib><creatorcontrib>Angeles‐Floriano, Tania</creatorcontrib><creatorcontrib>Parra‐Ortega, Israel</creatorcontrib><creatorcontrib>Gaytán‐Morales, Félix</creatorcontrib><creatorcontrib>Castorena‐Villa, Iván</creatorcontrib><creatorcontrib>López‐Martínez, Briceida</creatorcontrib><creatorcontrib>Ortiz‐Navarrete, Vianney</creatorcontrib><creatorcontrib>Olvera‐Gómez, Irlanda</creatorcontrib><title>Presence of antibodies against HLA class I and class II molecules in children before and after allo‐HSCT. Alloantibodies before and after HSCT</title><title>HLA</title><addtitle>HLA</addtitle><description>A severe complication of allogeneic hematopoietic stem cell transplantation (HSCT) is graft failure (GF). Among others, donor‐specific anti‐HLA antibodies (DSA) are associated with graft rejection after allogeneic or haploidentical transplantation in adults. Knowledge of DSA and pediatric recipients is limited. Hence, we aimed to generate more information about the presence of DSA (pre‐ and post‐HSCT) and the clinical outcomes (graft rejection and poor function) in children. We identified DSA in 27% of the patients. We observed a higher frequency (50%) of DSA‐bearing patients with a benign disease diagnosis than those diagnosed with leukemia (16.66%). We observed graft rejection in one patient (with DSA against two alleles of HLA class I molecules) and poor function in three recipients during the first 30 days after HSCT in the absence of DSA. The presence of donor and nondonor HLA‐specific antibodies decreased substantially after transplantation. After the transplant, we identified two patients with DSA specific for HLA class I molecules (independent of clinical relevance), and four recipients showed PGF in the absence of DSA. We were unable to establish any association between the presence of DSA and a clinical outcome: graft failure or prevalence of viral infection.</description><subject>Alleles</subject><subject>alloantibodies</subject><subject>Child</subject><subject>graft failure</subject><subject>Hematopoietic Stem Cell Transplantation</subject><subject>Histocompatibility Antigens Class I</subject><subject>Histocompatibility Antigens Class II</subject><subject>Humans</subject><subject>Isoantibodies</subject><subject>poor function</subject><subject>viral infections</subject><issn>2059-2302</issn><issn>2059-2310</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10MFKwzAcBvAgihtzB19AcvXQLUmTZjmWoW4wVHCeS5omGsjakXTIbj7CntEnMVvdEMRc8g_58YV8AFxjNMJxjVtZjzCdYH4G-gQxkZAUo_PTjEgPDEOwJSKZ4Cjj4hL00gwjJFjWB7tnr4OulYaNgbJubdlUVgco36StQwtnixwqJ0OA83hdHec5XDVOq42L1NZQvVtXeV3DUpvG64OUptUeSuear8_d7GW6HME8Hn698Qfv1RW4MNIFPfzZB-D1_m45nSWLp4f5NF8kimDGE8x0StUEpyb-yiAqUiQFZaakZYUQ40JxhjnNEMOlwJpUVFQpJkpSwpEkOB2A2y5X-SYEr02x9nYl_bbAqNgXW8Rii0Ox0d50dr0pV7o6yWONEYw78GGd3v6fVCzzxy7yG2aZgdc</recordid><startdate>202301</startdate><enddate>202301</enddate><creator>Morán‐Espinosa, Maricarmen</creator><creator>Angeles‐Floriano, Tania</creator><creator>Parra‐Ortega, Israel</creator><creator>Gaytán‐Morales, Félix</creator><creator>Castorena‐Villa, Iván</creator><creator>López‐Martínez, Briceida</creator><creator>Ortiz‐Navarrete, Vianney</creator><creator>Olvera‐Gómez, Irlanda</creator><general>Blackwell Publishing Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>202301</creationdate><title>Presence of antibodies against HLA class I and class II molecules in children before and after allo‐HSCT. Alloantibodies before and after HSCT</title><author>Morán‐Espinosa, Maricarmen ; Angeles‐Floriano, Tania ; Parra‐Ortega, Israel ; Gaytán‐Morales, Félix ; Castorena‐Villa, Iván ; López‐Martínez, Briceida ; Ortiz‐Navarrete, Vianney ; Olvera‐Gómez, Irlanda</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2157-15e34c813f697f04930a945fb4bd00579c751746051b91e2d49d312ca4270a213</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Alleles</topic><topic>alloantibodies</topic><topic>Child</topic><topic>graft failure</topic><topic>Hematopoietic Stem Cell Transplantation</topic><topic>Histocompatibility Antigens Class I</topic><topic>Histocompatibility Antigens Class II</topic><topic>Humans</topic><topic>Isoantibodies</topic><topic>poor function</topic><topic>viral infections</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Morán‐Espinosa, Maricarmen</creatorcontrib><creatorcontrib>Angeles‐Floriano, Tania</creatorcontrib><creatorcontrib>Parra‐Ortega, Israel</creatorcontrib><creatorcontrib>Gaytán‐Morales, Félix</creatorcontrib><creatorcontrib>Castorena‐Villa, Iván</creatorcontrib><creatorcontrib>López‐Martínez, Briceida</creatorcontrib><creatorcontrib>Ortiz‐Navarrete, Vianney</creatorcontrib><creatorcontrib>Olvera‐Gómez, Irlanda</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>HLA</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morán‐Espinosa, Maricarmen</au><au>Angeles‐Floriano, Tania</au><au>Parra‐Ortega, Israel</au><au>Gaytán‐Morales, Félix</au><au>Castorena‐Villa, Iván</au><au>López‐Martínez, Briceida</au><au>Ortiz‐Navarrete, Vianney</au><au>Olvera‐Gómez, Irlanda</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Presence of antibodies against HLA class I and class II molecules in children before and after allo‐HSCT. Alloantibodies before and after HSCT</atitle><jtitle>HLA</jtitle><addtitle>HLA</addtitle><date>2023-01</date><risdate>2023</risdate><volume>101</volume><issue>1</issue><spage>16</spage><epage>23</epage><pages>16-23</pages><issn>2059-2302</issn><eissn>2059-2310</eissn><abstract>A severe complication of allogeneic hematopoietic stem cell transplantation (HSCT) is graft failure (GF). Among others, donor‐specific anti‐HLA antibodies (DSA) are associated with graft rejection after allogeneic or haploidentical transplantation in adults. Knowledge of DSA and pediatric recipients is limited. Hence, we aimed to generate more information about the presence of DSA (pre‐ and post‐HSCT) and the clinical outcomes (graft rejection and poor function) in children. We identified DSA in 27% of the patients. We observed a higher frequency (50%) of DSA‐bearing patients with a benign disease diagnosis than those diagnosed with leukemia (16.66%). We observed graft rejection in one patient (with DSA against two alleles of HLA class I molecules) and poor function in three recipients during the first 30 days after HSCT in the absence of DSA. The presence of donor and nondonor HLA‐specific antibodies decreased substantially after transplantation. After the transplant, we identified two patients with DSA specific for HLA class I molecules (independent of clinical relevance), and four recipients showed PGF in the absence of DSA. We were unable to establish any association between the presence of DSA and a clinical outcome: graft failure or prevalence of viral infection.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>36100956</pmid><doi>10.1111/tan.14817</doi><tpages>8</tpages></addata></record> |
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subjects | Alleles alloantibodies Child graft failure Hematopoietic Stem Cell Transplantation Histocompatibility Antigens Class I Histocompatibility Antigens Class II Humans Isoantibodies poor function viral infections |
title | Presence of antibodies against HLA class I and class II molecules in children before and after allo‐HSCT. Alloantibodies before and after HSCT |
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