Abstract
Human monocyte-macrophages (MØ) mediate both spontaneous cytotoxicity (MØ-SCT) and antibody-dependent cell-mediated cytotoxicity (MØ-ADCC) against human fibroblasts (HF) infected with type 1 herpes simplex virus (HSV), and produce a characteristic type 1 human leukocyte-derived interferon (Hu IFN-α). The MØ-SCT and MØ-ADCC display distinctive reaction kinetics and effector cell-to-target cell (E:T) ratios. Interferon (IFN) production parallels the kinetics and E:T for MØ-SCT, and occurs irrespective of the presence of HSV-immune serum, suggesting that the induction of MØ IFN requires only that MØ encounter HSV-infected HF. The MØ IFN appears to be a by-product rather than a requirement for the MØ-SCT reaction, since anti-Hu IFN-α globulin neutralizes the antiviral activity of IFN but does not affect the MØ-SCT. An 18-hr preincubation of MØ with polyinosinic-polycytidylic acid (poly(I:C)) or with exogenous Hu IFN-a augments the MØ-SCT. It is postulated that the MØ-produced IFN could function to recruit subsequent MØ to become cytotoxic or augment natural-killer cell activity. Furthermore, enhancement of MØ-SCT by either poly(I:C) or IFN may present an alternative means of IFN therapy.
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