HLA Laboratory

Nantes, France

HLA Laboratory

Nantes, France

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Morishima S.,Aichi Cancer Center Hospital | Ogawa S.,University of Tokyo | Matsubara A.,University of Tokyo | Kawase T.,Aichi Cancer Center Research Institute | And 8 more authors.
Blood | Year: 2010

Although the effects of human leukocyte antigen (HLA) locus matching on clinical outcome in unrelated hematopoietic stem cell transplantations have been characterized, the biologic implications of HLA haplotypes have not been defined. We demonstrated the genetic fixity of Japanese conserved extended haplotypes by multi-single nucleotide polymorphism analysis in 1810 Japanese donor-recipient pairs matching with HLA-A, -B, -C, -DRB1, and -DQB1 alleles. Three major Japanese conserved extended haplotypes (named HP-P1, HP-P2, and HP-P3) were essentially completely conserved at least in the 3.3-Mb HLA region from HLA-A to -DPB1, and extended far beyond HLA-A. The risk of acute graft-versus-host disease (GVHD) of these HLA haplotypes was assessed with multivariate Cox regression in 712 patients transplanted from HLA fully (HLA-A, B, C, DRB1, DQB1, and DPB1) matched unrelated donors. HP-P2 itself reduced the risk of grade 2 to 4 acute GVHD (hazard ratio [HR] = 0.63; P = .032 compared with HP-P2-negative), whereas HP-P3 tended to increase the risk (HR = 1.38; P = .07). Among 381 patients with HP-P1, HP-P1/P3 (HR = 3.35; P = .024) significantly increased the risk of acute GVHD compared with homozygous HP-P1. This study is the first to demonstrate that a genetic difference derived from HLA haplotype itself is associated with acute GVHD in allogeneic hematopoietic stem cell transplantation. © 2010 by The American Society of Hematology.


Dabin T.,Peking Union Medical College | Jue W.,Peking Union Medical College | Guojin O.,Peking Union Medical College | Xingjie L.,HLA Laboratory | Qiang C.,Peking Union Medical College
Tissue Antigens | Year: 2014

The novel allele HLA-DPB1*04:01:15 is different from DPB1*04:01:01:01 with one nucleotide at nt 351 (C>A) in exon 2. © 2014 John Wiley & Sons A/S.


Dabin T.,Peking Union Medical College | Jue W.,Peking Union Medical College | Guojin O.,Peking Union Medical College | Hai Z.,HLA Laboratory | And 2 more authors.
Tissue Antigens | Year: 2014

HLA-A*02:463 differs from HLA-Az.ast;02:03:01 by one nucleotide at nt 334 A→G in exon 2. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.


Fleischhauer K.,Instituto Of Ricovero E Cura A Carattere Scientifico Irccs H San Raffaele | Shaw B.E.,The Institute of Cancer Research | Shaw B.E.,Royal Free Hospital | Gooley T.,Fred Hutchinson Cancer Research Center | And 14 more authors.
The Lancet Oncology | Year: 2012

Background: The risks after unrelated-donor haemopoietic-cell transplantation with matched HLA-A, HLA-B, HLA-C, HLA-DRB1, HLA-DQB1 alleles between donor and recipient (10/10 matched) can be decreased by selection of unrelated donors who also match for HLA-DPB1; however, such donors are difficult to find. Classification of HLA-DPB1 mismatches based on T-cell-epitope groups could identify mismatches that might be tolerated (permissive) and those that would increase risks (non-permissive) after transplantation. We did a retrospective study to compare outcomes between permissive and non-permissive HLA-DPB1 mismatches in unrelated-donor haemopoietic-cell transplantation. Methods: HLA and clinical data for related-donor transplantations submitted to the International Histocompatibility Working Group in haemopoietic-cell transplantation were analysed retrospectively. HLA-DPB1 T-cell-epitope groups were assigned according to a functional algorithm based on alloreactive T-cell crossreactivity patterns. Recipients and unrelated donors matching status were classified as HLA-DPB1 match, non-permissive HLA-DPB1 mismatch (those with mismatched T-cell-epitope groups), or permissive HLA-DPB1 mismatch (those with matched T-cell-epitope groups). The clinical outcomes assessed were overall mortality, non-relapse mortality, relapse, and severe (grade 3-4) acute graft-versus-host disease (aGvHD). Findings: Of 8539 transplantations, 5428 (64%) were matched for ten of ten HLA alleles (HLA 10/10 matched) and 3111 (36%) for nine of ten alleles (HLA 9/10 matched). Of the group overall, 1719 (20%) were HLA-DPB1 matches, 2670 (31%) non-permissive HLA-DPB1 mismatches, and 4150 (49%) permissive HLA-DPB1 mismatches. In HLA 10/10-matched transplantations, non-permissive mismatches were associated with a significantly increased risk of overall mortality (hazard ratio [HR] 1·15, 95% CI 1·05-1·25; p=0·002), non-relapse mortality (1·28, 1·14-1·42; p<0·0001), and severe aGvHD (odds ratio [OR] 1·31, 95% CI 1·11-1·54; p=0·001), but not relapse (HR 0·89, 95% CI 0·77-1·02; p=0·10), compared with permissive mismatches. There were significant differences between permissive HLA-DPB1 mismatches and HLA-DPB1 matches in terms of non-relapse mortality (0·86, 0·75-0·98; p=0·03) and relapse (1·34, 1·17-1·54; p<0·0001), but not for overall mortality (0·96, 0·87-1·06; p=0·40) or aGvHD (OR 0·84, 95% CI 0·69-1·03; p=0·09). In the HLA 9/10 matched population, non-permissive HLA-DPB1 mismatches also increased the risk of overall mortality (HR 1·10, 95% CI 1·00-1·22; p=0·06), non-relapse mortality (1·19, 1·05-1·36; p=0·007), and severe aGvHD (OR 1·37, 95% CI 1·13-1·66; p=0·002) compared with permissive mismatches, but the risk of relapse was the same in both groups (HR 0·93, 95% CI 0·78-1·11; p=0·44). Outcomes for HLA 10/10-matched transplantations with non-permissive HLA-DPB1 mismatches did not differ substantially from those for HLA 9/10-matched transplantations with permissive HLA-DPB1 mismatches or HLA-DPB1 matches. Interpretation: T-cell-epitope matching defines permissive and non-permissive HLA-DPB1 mismatches. Avoidance of an unrelated donor with a non-permissive T-cell-epitope mismatch at HLA-DPB1 might provide a practical clinical strategy for lowering the risks of mortality after unrelated-donor haemopoietic-cell transplantation. Funding: National Institutes of Health; Associazione Italiana per la Ricerca sul Cancro; Telethon Foundation; Italian Ministry of Health; Cariplo Foundation; National Cancer Institute; National Heart, Lung and Blood Institute; National Institute of Allergy and Infectious Diseases; Office of Naval Research; IRGHET Paris; Swedish Cancer Society; Children's Cancer Foundation; Swedish Research Council; Cancer Society in Stockholm; Karolinska Institutet; and Leukemia and Lymphoma Society. © 2012 Elsevier Ltd.


Yoshihara S.,Hyogo College of Medicine | Taniguchi K.,Hyogo College of Medicine | Ogawa H.,Hyogo College of Medicine | Saji H.,HLA Laboratory
Bone Marrow Transplantation | Year: 2012

The role of HLA antibodies in SCT has drawn increasing attention because of the significantly increased number of patients who receive HLA-mismatched SCT, including cord blood transplantation, haploidentical SCT and unrelated SCT. Technical advancements in the methods of HLA Ab testing have realized rapid, accurate and objective identification, as well as quantification of specific HLA antibodies. Recent clinical studies have suggested that the presence of donor-specific HLA antibodies (DSA) in patients is associated with graft failure in HLA-mismatched SCT when the above-listed stem cell sources are used and results in different impacts. Of note, most of the HLA-matched unrelated SCT actually involve HLA mismatches in HLA-DP and the presence of antibodies against this locus has been reported to be associated with graft failure. Thus, HLA Ab should be examined as a work-up for all patients who undergo SCT from alternative donors. The simplest route for preventing HLA Ab-mediated graft failure in Ab-positive patients is to avoid donors who possess the target Ag of HLA antibodies. If SCT from such donors must be performed, treatment for DSA before SCT may improve the chances of successful donor engraftment. © 2012 Macmillan Publishers Limited.


Endres R.O.,HLA Laboratory | Redman H.,HLA Laboratory | Marcus N.,HLA Laboratory
Tissue Antigens | Year: 2010

Cw*0774 differs from Cw*070201 by one nucleotide within the coding sequence of exons 2-4. DQB1*060105 differs from DQB1*060101 by one nucleotide within the coding sequence of exons 2-3. © 2009 John Wiley & Sons A/S.


Ou G.,Institute of Blood Transfusion | Wang J.,Institute of Blood Transfusion | Wang C.,Institute of Blood Transfusion | Ji X.,Institute of Blood Transfusion | Chen Q.,HLA Laboratory
Tissue Antigens | Year: 2014

The novel allele B*15:325 shows difference from B*15:02:01 at codon 127 resulting in changes from Asn to Ser. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.


Endres R.O.,HLA Laboratory
Tissue antigens | Year: 2013

Characterization of the novel HLA B*18:79 allele is described. © 2012 John Wiley & Sons A/S.


Endres R.O.,HLA Laboratory | Hoffman A.D.,HLA Laboratory | Scott I.,HLA Laboratory
Tissue Antigens | Year: 2012

A*03:132 differs from A*03:01:01:01 at nucleotide 853 (codon 261) in exon 4. © 2011 John Wiley & Sons A/S.


Wang C.,Institute of Blood Transfusion | Wang J.,Institute of Blood Transfusion | Ou G.,Institute of Blood Transfusion | Ji X.,Institute of Blood Transfusion | And 3 more authors.
Tissue Antigens | Year: 2015

The new allele HLA-DPB1*363:01 most closely resembles DPB1*92:01, differing at a single position 191 (exon 2, codon 35). © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

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