Platelets made HLA deficient by acid treatment aggregate normally and escape destruction by complement and phagocytes in the presence of HLA antibodies
Blood Platelets
Male
Phagocytes
Platelet Aggregation
Complement System Proteins
Hydrogen-Ion Concentration
Citric Acid
03 medical and health sciences
0302 clinical medicine
HLA Antigens
Humans
Female
DOI:
10.1111/trf.13350
Publication Date:
2015-10-07T06:14:30Z
AUTHORS (7)
ABSTRACT
BACKGROUND The presence of antibodies against HLA Class I can lead to platelet (PLT) transfusion refractoriness, that is, the repeated failure achieve adequate posttransfusion PLT count increments. refractoriness be overcome by HLA‐matched donor PLTs. A different approach is remove from surface using low pH. Previous case studies HLA‐stripped PLTs showed encouraging but inconsistent results and lacked information on biologic effects acid treatment function as well sensitivity destruction in antibodies. STUDY DESIGN AND METHODS prepared buffy coats were stripped a brief incubation at pH 2.9. Kinetics stripping, viability, phenotypic alterations, complement‐mediated lysis phagocytosis determined flow cytometry. Functional potential was evaluated multiplate analyzer. RESULTS Acid‐treated viable, upregulated activation markers normally aggregated similar extent untreated response stimulation with three natural agonists. Acid removed 70% 90% complexes surface, which led complete protection antibody–mediated complement reduced monocyte‐mediated anti‐HLA vitro. CONCLUSION Our study fills an important knowledge gap how affects interactions immune cells, paving way for controlled clinical trials evaluate acid‐treated alternative donors refractoriness.
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