A Gamma Interferon Independent Mechanism of CD4 T Cell Mediated Control of M. tuberculosis Infection in vivo
Figure 1
Mutation in amino acid 12 of ESAT6 prevents protection by C7 effector cells.
(A) Naïve C7 CD4 T cells were cultured in the presence of irradiated APCs (T cell depleted splenocytes) and either native ESAT6 peptide (aa 1–20) or mutated ESAT6 peptide in which amino acid number 12 was changed from glutamic acid to alanine (E12A). Analysis of tritiated thymidine incorporation reveals C7 CD4 T cells do not respond to ESAT6 (E12A). (B) B6 mice were infected with the indicated strains of Mtb and CFUs determined. Each dot represents data from 4–10 mice. (C) Bacterial numbers from mice that received Th1-skewed C7 effector cells and were subsequently infected with Δesat6+wt or Δesat6+E12A. Bacterial numbers were determined 21 days post infection.