direct tumor cell killing, antibody-dependent NK-mediated tumor killing). In vitro analyses showed that engagement of CR3 with iC3b (classical CR3 ligand) on NK cells negatively regulated NK cell activity and effector functions (i.e. In addition, adaptive transfer of NK cells lacking CR3 (into NK-deficient mice) mediated more efficient suppression of tumor growth and metastases, compared with the transfer of CR3 sufficient NK cells, suggesting that CR3 can impair tumor surveillance through suppression of NK cell function. In a B16-luc melanoma-induced lung tumor growth and metastasis model, mice deficient in CR3 had reduced tumor growth and metastases, compared with WT mice. Mice deficient in CR3 (CD11b−/− mice) exhibited a more activated NK phenotype and had enhanced NK-dependent tumor killing. Here, we show that CR3 is an important negative regulator of NK cell function, which has negative impact on tumor surveillance. Complement receptor 3 (CR3) is expressed abundantly on natural killer (NK) cells however, whether it plays roles in NK cell-dependent tumor surveillance is largely unknown.
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