Enhanced priming of adaptive immunity by a proapoptotic mutant of Mycobacterium tuberculosis
J. Clin. Invest. 117:8 doi:10.1172/JCI31947 [Go to this article.]

Figure 2
Enhanced CD8⁺ T cell activation in vivo by ΔsecA2.

(A) Mice were infected i.v. with the indicated bacterial strains, and spleens were harvested after 7 days for quantitation of SIINFEKL-specific T cells by IFN-γ ELISPOT. SFC, spot-forming cells. (B) CTL activity was measured in vivo by transfer of a mixture of SIINFEKL-pulsed CFSE^low and unpulsed CFSE^high splenocytes into recipient mice 14 days after infection with the indicated bacteria. Relative proportions of CFSE^low and CFSE^high were quantitated by FACS to determine percent specific lysis. (C) CD4⁺ T cell responses were unaffected by deletion of secA2. Seven days after infection with indicated bacteria, responses of splenocytes to purified protein derivative (PPD) and peptide-25 (Pep25) were determined by ELISPOT. (D) Thy1.1⁺ B6.PL mice were injected with CFSE-labeled Thy1.2⁺ OT-I splenocytes, and infected with the indicated bacteria. CD8⁺ T cell activation was assessed 6 days after infection by CFSE dilution. Dot plots show representative mice, and bar graphs show means and SDs for percentages of undivided cells in the transferred population for 2 or 3 mice per bacterial strain. (E) The enhanced CD8⁺ T cell proliferation induced by ΔsecA2 was reversed by reexpression of SodA secretion in the ΔsecA2-αsodA strain. Dot plots show CFSE dilution in the transferred population 6 days after infection with the indicated strains. The bar graph on the right shows means and SDs of the percentages of undivided cells for groups of 4 mice infected with each bacterial strain. All results are representative of at least 2 independent experiments.