DEFECTIVE CHEMOTACTIC FACTOR-INDUCED MONOCYTE COMPLEMENT RECEPTOR ENHANCEMENT IN LUNG-CANCER

  • 1 January 1983
    • journal article
    • research article
    • Vol. 54  (3) , 785-792
Abstract
Monocyte complement [component](C3b) rosettes, and chemotactic factor(CF)-induced enhancement of rosettes were studied in 37 patients with bronchial carcinoma (BC). These findings were compared to those obtained from 9 age- and sex-matched patients with nonmalignant respiratory disease (NMRD) and 38 normal healthy controls (HC). No differences in monocyte C3b rosettes were found when BC was compared with NMRD or HC. There was a highly significant inhibition of CF-induced complement receptor enhancement (CRE) in monocytes from patients with extensive or metastatic BC compared to NMRD or HC. These differences increased with time of incubation and concentrations of CF, and occurred when either f-Met-Leu-Phe, leukotriene B4 (LTB4) or casein were used as the enhancing agent. The defect in monocyte CRE was related to the stage of the disease (with the rank order, metastatic > confined to chest > localized tumor) but not to the pathohistologic type. A similar impairment in CRE was observed when neurophils from BC were compared to HC. In patients with advanced bronchial carcinoma, monocyte and neutrophil C3b receptors may have impaired responsivness to chemotactic factors.