Fig. 1. Flow cytometry assay to monitor the binding of selected aptamers with H37Rv (target bacteria) and BCG (negative bacteria). Compare with the background binding of unselected DNA library. For H37Rv, there was an increase in binding capacity of the aptamer NK2, whereas there was little change for the control BCG.

Fig. 2. Isothermal titration calorimetry (ITC) measurement of aptamer (NK2)–MTB interactions. (A) aptamer (NK2)–H37Rv interaction; (B) aptamer (NK2)–BCG interaction.

Fig. 3. Binding of aptamer NK2 to trypsin-treated or proteinase K-treated H37Rv.

Fig. 4. The effect of aptamer NK2 against Mycobacterium tuberculosis in vitro and vivo. (A) The intracellular IFN-γ levels increased in CD3⁺CD4⁺T cells in the presence of the aptamer NK2. (B) Aptamer NK2 enhances the survival rate of H37Rv-infected mice, statistical analysis using the Kaplan–Meier method, and statistical analyses of survival curves used a Breslow test (^*P < 0.05); (C) determination of CFU from lung and spleen of infected mice with or without aptamers treatment. Colony counts were determined after 4-weekly incubation at 37 °C and represented with log CFU. (D) Histopathological examination of biopsy specimens from lung in mice (HE, 10×). Data are presented as means ± standard error of the mean (SEM) and were analyzed using one-way analysis of variance (ANOVA) followed by Student–Newman–Keuls (SNK) post hoc test (^*P < 0.05).