C1qRp elicits a Ca++ response in rat NK cells but does not influence NK-mediated cytotoxicity.

Abstract

The cell surface receptor C1qRp (receptor for C1q, regulating phagocytosis) present on macrophages and neutrophils, is presumed to stimulate phagocytosis in these cells. However, C1qRp is also present on natural killer (NK) cells, and in these cells its physiological function is not currently known. We have investigated putative functions of this cell surface molecule in rat NK cells with the aid of two novel monoclonal antibodies (MoAb) LOV3 and LOV8 against rat C1qRp. NK cells are known to be potent cytotoxic effector cells, both through specific recognition of ligands on a target cell and killing of antibody-coated target cells (antibody-dependent cellular cytotoxicity, ADCC). NK cells prestimulated with MoAbs LOV3 or LOV8 did not exhibit altered ADCC. Furthermore, the addition of MoAb LOV3 or LOV8 to cytotoxic cultures of NK cells and Fc-receptor positive tumour cells did not affect killing in a redirected killing assay, indicating that the receptor did not influence NK cytotoxicity. However, this is the first paper to show that an intracellular Ca++-response is induced in rat NK cells upon stimulation of C1qRp with LOV3 and LOV8. The response induced by the antibodies was only minimally reduced in the presence of EGTA, indicating that most of the response is owing to the Ca++ mobilization from intracellular calcium stores.