PLATELET RESPONSE TO IMMUNOLOGICAL INJURY

Abstract

Platelets are susceptible to innnunological destruction, but the nature of the immune lesion has not been defined. Biochemistry, physiology, freeze-etching and electron microscopy were used to detect antibody induced injury. Antiserum (AS) was raised in a horse by repeated I.M. injections of glutaraldehyde fixed human platelets. Absorbtion with PPP removed non-specific activity of AS. The AS caused release of serotonin to a dilution of 1:10,000 without producing ultrastructural damage. AS stimulated aggregation in stirred C-PRP to a dilution of 1:1000. Aggregates resembled those produced by collagen. Lactic dehydrogenase was not discharged by dilutions greater than 1:10. Dilutions to 1:100 caused platelet lysis and produced characteristic membrane lesions visible in replicas of freeze-etched cells. The lesions consisted of 80A° particles in semi-circular or circular arrangements located on the inner surface of the outer leaflet, but not on the outer surface of the inside half of the split lipid bilayer. Complement was required for development of the lesions. Anti-lymphocyte serum strongly active against human platelets produced similar lesions, but antisera to rabbit platelets raised in a goat did not. The results indicate that specific, complement-dependent lesions are produced in platelet membranes by lytic concentrations of AS. Smaller amounts of AS or other anti-platelet substances may cause aggregation and release serotonin without producing specific lesions.