• 1 January 1982
    • journal article
    • research article
    • Vol. 49 (1), 11-21
Abstract
Both endogenous and interferon (.LAMBDA.FN]-augmented NK activity of normal donors were compared with that of patients suffering from either multiple sclerosis (MS), systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA). Endogenous NK was assayed using an NK susceptible target cell (K562) [human leukemia cells], and augmented NK using a target cell (WI-L2) [human B lymphoblastoid cells] which is lysed only by NK effector cells that have been pre-stimulated by IFN or IFN-inducers. While NK function appeared normal in RA patients, the study confirms reports of defective endogenous NK in many MS and SLE patients. Anomalous IFN-augmented NK was also detected in many patients with these 2 diseases, indicating that defective NK function cannot always be corrected by IFN treatment in vitro. Analysis of IFN production, endogenous NK and IFN-augmented NK by individual patients with MS or SLE showed the defects in their IFN-NK systems to be highly selective, suggesting that individual components of this system may operate independently.