Platelets in allergy. Assays and interpretation.

Abstract

Since 1983, when we reported the first model of antiparasite activity by platelets, five different triggering processes have been described that induce these blood elements into the role of efficient killers of pathogens. Besides endogenous compounds, such as specific IgE antibodies, inflammatory CRP, IFNT, and a second stimulating lymphokine, provisionally termed PCIF, exogenous chemAcals have also been shown to express unexpected activating properties on uncommon platelet populations or in particular situations: aspirin and NSAID on platelets from asthmatics, and DEC on platelets from patients with filariasis. These various stimuli probably triggered thrombocytes by different pathways, but achieved a common result: the generation of cytocidal molecules. A general feature of the stimulating signals was apparently to induce cytotoxic properties without aggregation, suggesting that they triggered a platelet compartment that was not involved in classical activation by aggregating agents such as thrombine, adenosine diphosphate, or platelet-activating factor-acether. The hypothesis remains that the killing capacities of platelets were supported by specific subpopulations, either working on their own, or producing secondary mediators for the general participation of nonresponding platelet populations.