2006 Volume 52 Issue 5 Pages 589-598
It has been proposed that anti-platelet antibodies having the ability to induce platelet activation are involved in not only thrombocytopenic states, but also in the pathology of nonhemolytic transfusion reactions (NHTRs). Recently, we reported that anti-CD36 Abs-containing plasma, derived from the donor SS, was implicated in NHTRs, and induced platelet activation, suggesting the involvement of anti-CD36 Abs in the occurrence of NHTRs. In addition to the serum derived from donor SS (SS serum), one of 13 anti-CD36 Abs-containing sera (anti-CD36 sera) also caused platelet aggregation. The factors that determine the platelet-activating abilities of anti-CD36 sera might also influence the occurrence of anti-CD36 Abs-related NHTRs. In this study, we focused on the relationship between the anti-CD36 Ab titer in sera and the platelet-activating ability of sera to elucidate the determinants of the platelet-activating action of anti-CD36 sera.
Sixteen anti-CD36 sera (serum #1∼#15), including the SS serum, were incubated with CD36-positive or-negative platelets. Platelet aggregation, the RANTES release and the titer of anti-CD36 Abs in sera were then determined. The two sera (SS serum and serum #1) that induced CD36-specific platelet activation had higher titers (x512) of anti-CD36 Abs than the other sera (less than x128). When SS serum and serum #1 were diluted to a titer of x128, the platelet-activating ability was lost. Furthermore, a subthreshold dose of epinephrine potentiated the platelet aggregation induced by SS serum and serum #1 at a titer of x256 and x341, respectively. When diluted to a titer of x128, however, both sera, failed to induce aggregation even in presence of epinephrine. Similarly, there was no synergistic platelet activation by epinephrine and any of the other anti-CD36 sera showing a titer of x128 or less.
These findings demonstrated that the platelet-activating ability of anti-CD36 serum depends on the anti-CD36Ab titer, suggesting that the titer of anti-CD36 Abs in blood components may determine the occurrence of anti-CD36 Abs-related NHTRs.
