Endocytosis, storage, and release of IgE by human platelets: Differences in patients with type I allergy and nonatopic subjects

Platelets of atopic individuals differ in alpha-granular contents and in the amount of biologically active mediators released compared with platelets of nonatopic subjects, Because platelets carry the low-affinity IgE receptor (CD23), they may contribute to long-lasting IgE sensitivity by serving as a storage pool for IgE. We compared 45 atopic individuals with immediate-type allergies and 25 nonatopic control subjects with respect to storage and release of IgE by their platelets, Platelets of atopic individuals were characterized by a 10-fold higher median IgE content compared with those of nonatopic control subjects, The platelet IgE content correlated with the serum IgE level in the four atopic individuals with seasonal allergies who were followed up monthly over I year, Platelet stimulation with platelet activating factor, but not with thrombin or adenosine diphosphate, resulted in a release of 65% of the stored IgE. Conversely, platelet stimulation with monoclonal IgE/kappa resulted in the release of the chemokine RANTES. Platelet alpha-granules were identified as the main storage compartment for IgE by postembedding immunocytochemistry, Although more than half of the alpha-granules showed gold labeling for IgE, additional labeling was found on the external face of the plasma membrane and within the open canalicular system, indicating endocytosis and exocytosis of IgE, Moreover, the detection of CD23 not only on the plasma membrane but also on membranes of the alpha-granules further supports the existence of an exchange of IgE between the blood plasma and an internal storage compartment. Endocytosis could be confirmed by the uptake of an IgE myeloma protein coupled to colloidal gold. We conclude that platelets of atopic individuals may contribute to allergic inflammation by serving as a storage pool for IgE and by their increased capacity to liberate further mediators of allergy in response to IgE stimulation.