Background Platelet (PLT) transfusions are an essential treatment for bleeding disorders. However, immunologic complications can occur, including alloantibody production against Class I HLA molecules. The principal source of HLA molecules in PLT concentrates (PCs) is the PLTs themselves. However, extracellular microparticles (MPs) present in PCs may express HLA molecules. Study Design and Methods We used nanoscale flow cytometry to explore the expression of HLA‐A2, HLA‐B7, and HLA‐B57 on the surface of cells, PLT‐derived MPs (PMPs), lymphocyte‐derived MPs (LMPs), and monocyte‐derived MPs (MMPs) present in PCs. Expression was studied during 7 days of storage. Results Platelets were not the only source of HLA molecules in PCs. HLA molecules were present on PMPs, LMPs, and MMPs. The level of HLA Class I molecule expression varied between haplotypes and MPs of different origins and during storage. Conclusion Platelets or residual cells remaining after leukoreduction are not the only source of HLA Class I molecules in PCs, highlighting the contribution of MPs to alloimmunization mechanisms. These data may be relevant for the development of new transfusion guidelines.

Background: Patients with hematologic malignancies require prophylactic or curative platelet transfusions to prevent or treat bleeding. Treatments such as chemotherapy, radiotherapy, and hematopoietic stem cell transplantation cause persistent thrombocytopenia, necessitating platelet transfusions. However, class I HLA antibodies can cause a serious complication: immune-mediated platelet refractoriness. The mechanisms of alloimmunization are incompletely understood. We explored the immunogenicity of HLA molecules and the phenotype of the HLA-specific CD4 + T cells involved in alloimmunization. Study Design and Methods: We investigated the role of HLA molecules in platelet transfusion immunogenicity in a retrospective cohort study on men with specific anti-HLA who had undergone transfusion. We investigated the presence and phenotypic profile of HLA-specific CD4 + T cells in alloimmunized patients included in long-term platelet transfusion programs for hematologic malignancies. Results: More than 50% of the transfused subjects displayed an antibody response against HLA-B57 or-B58. HLA-B57-specific CD4 + T-cell responses were observed in patients alloimmunized against HLA-B57. Following specific stimulation, the patients presented HLA-specific CD4 + T cells producing tumor necrosis factor-α, interleukin (IL)-13, IL-17A, IL-2, IL-10, and IL-21. Conclusion: These results shed light on posttransfusion class I anti-HLA alloimmunization mechanisms and constitute a first step toward developing new strategies for reducing refractoriness.

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