Studies on platelets

Abstract 1.1. A attempt was made to induce platelet antibody production in rabbits by injection of antigenically modified platelets. Modification of platelets was attempted by: (a) washing and standing; (b) incubation with drugs (aminopyrine, quinine, quinidine); (c) treatment with bacterial filtrates (Streptococcus hemolyticus and Staphylococcus albus and aureus); (d) treatment with Newcastle disease virus. Treated platelets were injected into 3 groups of rabbits; one received human platelets (heterologous immunization), one received platelets from normal rabbits (isoimmunization), and the third group received their own platelets (autoimmunization). Development and specificity of platelet agglutinins were evaluated by standard immunologic methods in vivo and in vitro. 2.2. High titer heteroimmune agglutinins developed constantly against human platelets. There was not, however, evidence for a specific antigenicity of modified versus nonmodified platelets. In one animal a naturally occurring isoantibody decreased in titer as the heteroantibody developed. 3.3. Autoantibodies and isoantibodies were often detected in the serum of rabbits receiving their own modified platelets in the presence or in the absence of the modifying agent. Animals receiving isoimmunization failed, however, to develop specific antibodies in vitro. Changes in protein and glycoprotein electrophoretic pattern were noted in the serum of auto- and isoimmunized rabbits, which were similar to those obtained in other instances of experimental immunization. When the specific modifying agent was injected into auto- or isoimmnnized rabbits, significant thrombocytopenia followed in many instances. The state of immunization was short-lived (less than 3 months). Results of our experiments indicated the simultaneous development of isoimiminization and autoimmunization in the course of the injection of modified auto- or isoplatelets. 4.4. Experimental results were not constant and reproducible in all animals of any given group. This is quite in agreement with the observations in humans, where only a few individuals, among many, develop thrombocytopenia after exposure to drugs, bacteria, and viruses. 5.5. Some of the findings obtained in the course of these studies could be applied to the interpretation of the pathogenesis of some thrombocytopenic states in man.