Are human platelet alloantigens (HPA) minor transplantation antigens in clinical bone marrow transplantation?
Are human platelet alloantigens (HPA) minor transplantation antigens in clinical bone marrow transplantation?"
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The role of human platelet alloantigens (HPA) in clinical bone marrow allotransplantation was investigated. The leading hypothesis was that HPA alloepitopes act as minor histocompatibility
antigens and aggravate graft-versus-host disease (GVHD). To exclude the effect of MHC disparity, only HLA identical donor-recipient pairs were entered into the study. The influence of HPA
compatibility on overall survival, occurrence of relapses and haematopoietic recovery was also investigated. A total of 223 patients who received a graft from an HLA-identical sibling,
genotyped for HPA -1, -2, -3, -4 and -5, were observed over a post-transplant period of 24 months following the protocol recommended by EBMT. The data from patients having received grafts
from HPA compatible donors were compared to data from patients having received grafts that were mismatched in HPA allotypes in the GVH direction. Analysis of the incidence of acute and
chronic (GVHD), overall survival, relapse incidence, haematopoietic recovery and some other clinical parameters did not reveal any significant difference between the HPA-matched and
-mismatched groups of patients, regardless of their age. Our results give no evidence that HPA-1, -2, -3 and -5 alloantigens should be considered minor transplantation antigens in clinical
bone marrow transplantation.
P Rožman, M Karas, A Košir, B Labar, A Madrigal, D Middleton, C Navarrete, M Oudshoorn, H Schennach, A Vitek and M Bohinjec: Members of Collaborative study P Rožman, M Bohinjec, A Košir, T
Dovč, T Ficko, B Vidan-Jeras and M Jeras (Blood Transfusion Centre of Slovenia, Ljubljana); J Pretnar and J Jazbec (Clinical Centre Ljubljana); M Oudshoorn and A-M van Walraven (Europdonor
Foundation, Leiden); M Karas and P Jindra (Charles University Hospital, Plzen); A Vitek and I Karlachova (Institute of Hematology and Blood Transfusion, Praga); H Schennach, A Schmarda
(Central Institute for Blood Transfusion and Immunology Department, General Hospital and University Clinics, Innsbruck) and D Nachbaur (Department of Internal Medicine, University Hospital,
Innsbruck) B Labar, A Kaštelan, M Pisk, E Čečuk, B Golubić and Z Ivanković (Clinical Center Rebro, Zagreb); D Middleton (Northern Ireland Regional Histocompatibility and Immunogenetics
Laboratory, City Hospital, Belfast) and M-F McMullin (Department of Haematology, Royal Victoria Hospital and Queens University, Belfast); C Navarrete and D Sage (North London Blood
Transfusion Centre, London); A Madrigal and A Pay (Anthony Nolan Research Institute, London)
Northern Ireland Regional Histocompatibility and Immunogenetics Laboratory, City Hospital, Belfast
Central Institute for Blood Transfusion and Immunology Department, General Hospital and University Clinics, Innsbruck
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