Peripheral blood granulocytes from normal, healthy donors and from two patients with chronic granulomatous disease were shown to significantly and reproduc-ibly inhibit the cytolytic capacity of autologous or allogeneic natural killer (NK) cells, when coincubated with these effector cells in either 4-hr or 18-hr 51chromium-release assays. Maximum inhibition was expressed by whole, intact granulocytes, although partial inhibition of NK cell activity was sometimes mediated by membrane fragments or soluble extracts obtained by sonication of granulocytes. In no experiment did supernatants from cultured granulocytes exhibit inhibitory activity. Although inhibition was directly proportional to the number of granulocytes present, our data indicate that inhibition by granulocytes was probably not due merely to steric interference in the assay, since granulocytes that had previously been exposed to heat (50°C, 30 min) maintained their capacity to inhibit NK in spite of losing all capacity to adhere to surfaces or to phagocytize particles. Further, inhibition was not due to cold-target inhibition of effector cells, ingestion of free 51Cr in the reaction mixture, or release by granulocytes of certain prostaglandins, reactive oxygen radicals, or iron-containing molecules. Granulocytes may act to inhibit NK cells via a potent heat-stable soluble factor, such as a protease inhibitor, which acts at short range in our in vitro tests. Although this latter concept remains conjecture, our in vitro data suggest that peripheral blood granulocytes may be able to exert, in vivo, a previously unrecognized regulatory effect on NK cells.
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Kay et al. (1983) studied this question.