The Destruction of Red Cells by Antibodies in Man. II. Pyrogenic, Leukocytic and Dermal Responses to Immune Hemolysis1

Abstract

Destruction of red cells by isoantibodies in normal human subjects was accompanied by a profound leukopenia, affecting granulocytes and monocytes. The abrupt, primarily hepatic, sequestration of ABO-incompatible red cells produced an abrupt leukopenia, while the slower, mainly splenic, sequestration of red cells coated with incomplete (anti-D) antibodies was accompanied by a synchronous, slowly developing leukopenia. In each instance there followed a leukocytosis, initially composed of immature granulocytes. Leukopenia did not appear during hemolysis in vitro by nonimmunologic mechanisms involving either hepatic or splenic filtration of red cells. Although injections of soluble A substance into subjects whose sera contained anti-A did provoke leukopenia, the reaction of isoantibodies with red cells affected leukocyte levels only when actual red cell sequestration or lysis transpired. Febrile reactions, like leukopenia, accompanied hemolysis in vivo by immune, but not by nonimmune, mechanisms. The intracutaneous injection of red cells into ABO-incompatible subjects manifesting hemolysins for these red cells in vitro provoked immediate, transient, local skin reactions consisting of wheal formation, erythema and venous constriction. Such reactions also followed intracutaneous injections of autogenous red cells hemolyzed in vitro beforehand by isoantibodies. It is believed that these dermal effects represent the release of histamine, serotonin and related compounds from leukocytes and platelets injured by immune hemolysis.