It remains unclear, why only some patients form alloantibodies against foreign RBC antigens. Transfusion of red blood cell (RBC) products and pregnancy are the most relevant causes of immunization against RBC alloantigens. Here we investigated the relationship between RBC alloantibodies, Rh phenotype, and HLA phenotype among patients with multiple RBC alloantibodies METHODS: In a group of 124 multi-responders-including both pregnant women and transplant recipients-we analysed the distribution of HLA-Class II variants in subgroups of multi-responders to RBC alloantigens according to their Rh status. RESULTS: As expected, the RhD-negative phenotype was overrepresented in our alloimmunized group (49.2 %) compared to in the general population. Importantly, HLA-DRB1*15 carriers were signifi cantly overrepresented among D-negative multi-responders compared to D-positive multi-responders (Pc = 0.045). Furthermore, the linked HLA-DRB1*13, HLA-DQB1*06, and HLA-DQA1*01 variants were more frequent in individuals with the DCCee phenotype than in other RhD-positive phenotypes. CONCLUSION: Our present fi ndings showed that RBC multispecifi c alloimmunization was associated with particular HLA-Class II variants based on Rh status (Tab. 3, Ref. 22).
Aseptic loosening and osteolysis are the most frequent causes of total hip or total knee arthroplasty failure. Osteolysis is induced predominantly by polyethylene particles that are produced by adhesive wear of the prosthesis. The particles trigger a complex host's reaction varying in intensity even in response to the same number of particles. These differences indicate that individual predisposition may have an important role in the pathogenesis of osteolysis. The major key mediators of wear-induced osteolysis include the cytokines RANKL, TNF-a, IL-1, IL-6 and IL-8. The inter-individual differences in the extent of bone destruction may therefore be related to variation in the amount and/or activity of these cytokines based on their gene polymorphism. Our pilot study suggests an association of some variants of the cytokine genes (e.g., IL1A-889) with a predisposition to development of severe osteolysis. If this assumption is confirmed by future investigations, this approach can facilitate the pre-operative identification of patients at risk of the development of severe periprosthetic osteolysis and premature failure of the implant.
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