JLE

Hématologie

MENU

HLA and blood transfusion Volume 6, issue 5, Septembre - Octobre 2000

Figures

See all figures

Author
Laboratoire d'immunologie, institut de biologie, centre hospitalier universitaire de Nantes, 9, quai Moncousu, 44035 Nantes cedex 01.

The HLA System is implicated in blood transfusion in several ways. As a highly polymorphic and immunogenic system, HLA is frequently involved in post-transfusionnal reactions, such as non hemolytic febrile reactions or transfusion related acute lung injury. HLA antibodies are not the only cause of these syndroms but they must be looked for in recipients and donors of suspected blood products. Leukocyte depletion or UV-B irradiation of cellular blood products are able to prevent both these reactions and the primary but not the secondary HLA alloimmunization. Anti-HLA immunization may also be involved in states of refractoriness to platelet transfusion. An appropriated selection of HLA compatible platelets can help restoring a convenient post-transfusion platelet recovery. As the major histocompatibility system, the HLA molecules could play a role in the favourable effect of blood transfusions given prior kidney transplantation, but the exact mechanism remains unknown. Non-leucodepleted transfused blood actually brings all cells able to elicit an allogenic immune response, usually involved in graft rejection. Immunogenetic conditions and mechanisms leading from this usual reactive state to an attenuated allo-immune response are far from being fully understood. In contrast the occurrence of a graft versus host disease in an immunocompetent recipient is a rare side effect of blood transfusion; it illustrates the deleterious effect of lacking HLA histoincompatibility between a donor and a recipient. In most cases this GVH reaction is due to the injection of blood from a homozygous donor for an HLA haplotype into an heterozygous recipient. As molecules involved in peptide presentation to T lymphocytes, HLA class II molecules play a role in the capacity to develop certain platelet alloantibodies reponsible for neonatal allo-immune thrombocytopenias or post-transfusion purpuras. The strongest association was established between anti-HPA-1a antibodies and HLA-DRB3*0101. In this case the ability of this HLA molecule to combined with the HPA-1a derived peptide rely upon the presence in this peptide of a leucine which is substituted by a proline in the HPA-1b allele. Thus HPA-1b homozygous people who are HLA-DRB3*0101 are at risk to develop anti-HPA-1a alloimmunization.