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Title: Complement bound to tumor target cells enhances their sensitivity to macrophage-mediated killing

Journal Article · · Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States)
OSTI ID:6915204

Tumor cells are known to be susceptible to destruction by a variety of immune effector mechanisms including complement (C) and activated macrophages (M theta). The authors have chosen to study the interaction of these two effector systems by examining the effects of bound mouse C on the antibody-independent M theta-mediated lysis of the P815 mouse mastocytoma cell line. Hemolytically active normal mouse serum (NMS) was used to deposit C on tumor targets by an alternative pathway mechanism in the absence of added antibody. C3 was quantitated on the P815 cells by a cellular enzyme-linked immunosorbant assay. C. parvum-activated macrophages produced tumor cytolysis which was measured in a serum-free 16 hour /sup 51/Cr-release assay. Target cells which had been incubated with NMS for 30 min at 37/sup 0/C demonstrated a 30% increase in specific /sup 51/Cr-release at a 1:1 effector to target (E:T) ratio, as compared to targets incubated with heat-inactivated (56/sup 0/C, 30 min) NMS. The treatment of target cells with NMS alone did not cause lysis. At higher E:T ratios specific /sup 51/Cr-release approached a maximum level which was not increased further by C treatment of the target cells. However, at low E:T ratios, NMS increased the specific /sup 51/Cr-release in a dose-dependent fashion; this increase was abrogated by 10 mM EDTA. The kinetics of lysis of C-treated P815 cells by activated M theta does not differ from that of control P815 cells. These results indicate that target-bound C may enhance M theta-mediated killing of tumor cells.

Research Organization:
Rush Medical Center, Chicago, IL
OSTI ID:
6915204
Report Number(s):
CONF-8604222-; TRN: 87-005977
Journal Information:
Fed. Proc., Fed. Am. Soc. Exp. Biol.; (United States), Vol. 45:4; Conference: 70. annual meeting of the Federation of American Society for Experimental Biology, St. Louis, MO, USA, 13 Apr 1986
Country of Publication:
United States
Language:
English