The mechanism behind the effect of ALG on platelets in vivo

Antilymphocyte globulin (ALG) and antiplatelet globulin (APG) were injected in dogs whose autologous platelets were labelled with 51Cr. APG injection resulted in almost complete and irreversible disappearance of labelled platelets. ALG produced thrombocytopenia of the same degree, but this was to a large extent reversible. After injection of ALG the platelets were reversibly trapped in the lung during the time when platelet count in peripheral blood was low. Such trapping was not seen after administration of APG. This suggests an antiplatelet mechanism of ALG quite different from that of APG. Platelet-absorbed ALG and non-platelet-absorbed ALG produced thrombocytopenia of the same degree and pattern, making it less likely that the thrombocytopenia was caused by specific platelet antibodies. Also platelet-absorbed APG induced thrombocytopenia, but this was reversible and 'ALG-like'. The mechanism behind the platelet reaction after an ALG injection is well explained in terms of complement C3 adherence and/or Fc receptor-induced aggregation.