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. Author manuscript; available in PMC: 2014 Jan 28.
Published in final edited form as: Angew Chem Int Ed Engl. 2012 Dec 11;52(5):1472–1476. doi: 10.1002/anie.201207063

Figure 3.

Figure 3

Aptamer-assisted immune effector cell targeting and killing of leukemia cells (a) NK-K562 cell binding assay. NK cells recognize K562 cells spontaneously; however, aptamer modification improved the targeting efficiency by 50%. (b) NK-K562 cell killing assay. Aptamer-modified NK cells killed K562 cells more efficiently, especially in the presence of background cells (Ramos). (c) CTL-Ramos cell binding assay. Without presenting the specific MHC1:peptide on Ramos cell surfaces, CTL cannot recognize Ramos cells. On the other hand, aptamer-modified CTL recognized 80% Ramos cells. (d) CTL-Ramos cell killing assay. Assisted by membrane-anchored aptamers, CTL targeted and killed Ramos cells via cell-mediated immunity. CTL-mediated cytotoxicity was confirmed by blocking the perforin/granzyme pathway with antibody. Values are means with SD (n=3). The single asterisk indicates a significant difference between aptamer-modified and unmodified or Lib-modified groups determined by the one-tailed t-test at P<0.01. The double asterisks indicate a significant difference between aptamer-modified and anti-Perforin treated groups determined by the one-tailed t-test at P<0.01.