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Blood, 1 November 2002, Vol. 100, No. 9, pp. 3304-3310
IMMUNOBIOLOGY
Expression of rat complement control protein Crry on tumor cells
inhibits rat natural killer cell-mediated cytotoxicity
Theresa A. Caragine,
Masaki Imai,
Alan B. Frey, and
Stephen Tomlinson
From the Department of Microbiology and Immunology,
Medical University of South Carolina, Charleston, SC, and the
Departments of Pathology and Cell Biology and Kaplan Cancer Center, New
York University School of Medicine, New York, NY.
Crry is a rodent membrane-bound inhibitor of complement activation
and is a structural and functional analog of the human complement
inhibitors decay-accelerating factor and membrane cofactor protein. We
found previously that expression of rat Crry on a human tumor cell line
enhances tumorigenicity in nude rats. In this study, we investigated
the effect that rat Crry expressed on tumor cells has on rat
cell-mediated cytotoxicity and antibody-dependent cell-mediated
cytotoxicity (ADCC). The expression of rat Crry on the surface of
different human tumor cell lines inhibited ADCC mediated by rat natural
killer (NK) cells. C3 opsonization is known to enhance NK
cell-mediated cytolysis, and a potential mechanism for Crry-mediated
inhibition of NK cell lysis is through Crry modulation of C3 deposition
on target cells. However, the transfection of tumor cell lines with
Crry enhanced their resistance to NK cell-mediated lysis in the
absence of exogenous complement. The resistance of Crry-expressing
tumor cells to NK cell-mediated ADCC could be reversed by treatment
with anti-Crry F(ab)2. In addition, anti-Crry
F(ab)2 enhanced the susceptibility of 13762 rat mammary
adenocarcinoma cells (that endogenously express Crry) to ADCC mediated
by allogeneic rat NK cells in the absence of added complement. We found
no evidence that rat NK cells were a source of complement for target
cell deposition during the in vitro cytolysis assay. These data suggest
a novel function for rat Crry in tumor immune surveillance that may be
unrelated to complement inhibition.
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