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Human Neutrophils Lose Their Surface FcyRIII and Acquire Annexin V Binding Sites During Apoptosis In Vitro

We have previously reported that neutrophilic granulocytes rapidly release part of their FcyRlll from the plasma membrane upon in vitro activation, probably by proteolytic cleav-age. In plasma and other body fluids, released or soluble FcyRlll has been found in considerable amounts. In the present study, neutrophils were kept in maintenance culture for 18 to 24 hours. Forty percent of the neutrophils completely lost FcyRIII, and the remainder of the cells showed a 60% decrease in FcyRlll expression on their surface. Released FcyRlll was detected in the culture supernatant. Neverthe- less, more than 90% of the cells was viable as judged by hydrolysis of fluorescein diacetate. The presence of inter- feron y, granulocyte colony-stimulating factor, or granulo-cyte-macrophage colony-stimulating factor, but not interleu-kin-3 (IL-3). IL-6, or IL-8, in the culture medium increased the number of cells that still expressed FcyRIII. We found that OLYMORPHONUCLEAR neutrophils play an important role in the inflammation process. As a first-line defense, neutrophils leave the circulation upon stimulation and enter the inflamed site to subsequently kill the invading micro-organisms. For this purpose, neutrophils express receptors on their plasma membranes for IgG antibodies and complement fragments present on opsonized micro-organ-isms. The receptors for the Fc region of IgG (FcyR) present on neutrophils are the transmembrane FcyRIIa and the PI-linked FcyRIIIb. In addition, neutrophils can be induced by certain cytokines to express the high-affinity FcyRI.