Anti-H can trigger apoptosis and down-regulate FUT1 expression in erythroid differentiated K562 cells without complement mediation.

The reason why delayed RBC engraftment and pure red cell aplasia (PRCA) develop only in some but not all recipients of major ABO-incompatible hematopoietic stem cell transplantation (HSCT) remains elusive and the underlying mechanisms are not fully understood. Understanding how incompatible erythroid blood group antibodies (Abs) interact with ABH antigens (Ags) of grafts, and investigating how to induce artificially accommodation of grafts are of obvious importance in transplantation immunology. The effects of anti-H on proliferation, apoptosis, and α-(1,2)-fucosyltransferase gene (FUTJ) expression in erythroid differentiated K562 cells were analyzed by the MTT assay, Annexin V/PI staining, and quantitative RT-PCR method. The growth of erythroid differentiated K562 cells was significantly suppressed when anti-H dilution was ≤1:8 (P< 0.001, as compared with 1:16). Under the complement-free culture conditions, the apoptotic ratio of erythroid differentiated K562 cells was significantly increased when anti-H dilution was ≤1:16 (P<0.05, as compared with 1:32). The apoptosis was not only closely associated with anti-H dilution (F = 138.991, P<0.001 ), but also correlated with treated time (F = 583.249, P<0.001 ), which indicated typical dose- and time-dependent effects. Under the complement-free culture conditions, the FUT1 mRNA expression level was also suppressed when anti-H dilution was ≤1:16 (P<0.05, as compared with 1:32), which also manifested in typical dose-dependent (F= 130.356, P<0.001) and time-dependent (F= 1432.00, P<0.001) effects. The results confirm that anti-H can trigger apoptosis and down-regulate FUT1 expression in erythroid differentiated K562 cells without complement mediation. The findings suggest that anti-H could accommodate grafts through triggering apoptosis and down-regulating Futl expression to reduce ABH antigens. [ABSTRACT FROM AUTHOR]