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CFDA-SE (5(6)-carboxyfluorescein diacetate succinimidyl ester) is a stable, cell-permeable diacetate precursor to CFSE. Upon diffusion into the cell, intracellular esterases cleave the acetate group to generate CFSE, which interacts with cellular amines via its succinimidyl groups to generate a highly fluorescent green dye that is impermeant to the cell membrane. CFDA-SE is frequently used in cell proliferation assays, as it is partitioned approximately equally between the progeny so that cell division can be followed as a successive halving of the fluorescence intensity through multiple generational divisions. CFDA-SE is also used for motility assays and in vivo cell tracking experiments. CFDA-SE-labeled cells can be detected with any instrument/filter set compatible with fluorescein detection.
(A) Flow cytometry analysis of Sp2/0 mouse myeloma cells labeled with CFDA-SE and analyzed by flow cytometry after being cultured for 0, 24, and 48 hours (filled histograms). Solid line histogram (control) shows unlabeled cells analyzed after 48 hours of cell culture. (B) Chemical structure of CFDA-SE.
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TLR9 agonism differentially impacts human NK cell-mediated direct killing and antibody-dependent cell-mediated cytotoxicity
A. Mahr et al.
Scientific Reports 2024 Jun
Abstract
There are two known mechanisms by which natural killer (NK) cells recognize and kill diseased targets: (i) direct killing and (ii) antibody-dependent cell-mediated cytotoxicity (ADCC). We investigated an indirect NK cell activation strategy for the enhancement of human NK cell killing function. We did this by leveraging the fact that toll-like receptor 9 (TLR9) agonism within pools of human peripheral blood mononuclear cells (PBMCs) results in a robust interferon signaling cascade that leads to NK cell activation. After TLR9 agonist stimulation, NK cells were enriched and incorporated into assays to assess their ability to kill tumor cell line targets. Notably, differential impacts of TLR9 agonism were observed—direct killing was enhanced while ADCC was not increased. To ensure that the observed differential effects were not attributable to differences between human donors, we recapitulated the observation using our Natural Killer—Simultaneous ADCC and Direct Killing Assay (NK-SADKA) that controls for human-to-human differences. Next, we observed a treatment-induced decrease in NK cell surface CD16—known to be shed by NK cells post-activation. Given the essential role of CD16 in ADCC, such shedding could account for the observed differential impact of TLR9 agonism on NK cell-mediated killing capacity.
