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. Author manuscript; available in PMC: 2011 Sep 9.
Published in final edited form as: Cell Microbiol. 2009 May 6;11(8):1170–1178. doi: 10.1111/j.1462-5822.2009.01335.x

Figure 1.

Figure 1

Mycobacterium tuberculosis (Mtb) inside the macrophage. In resting macrophages, Mtb stalls phagosome maturation and inhibits phagolysosome fusion. As a consequence, Mtb resides in a mildly acidic compartment and is exposed to reactive oxygen intermediates (ROI) from phagocyte oxidase (NOX2). Upon immunological activation with IFNγ the phagosome matures and fuses with lysosomes. This exposes Mtb to protons from the vacuolar ATPase, reactive nitrogen intermediates (RNI) from inducible nitric oxide synthase (iNOS) and ROI from NOX2. Mtb has evolved mechanisms to counter these interdependent forms of stress and allow its survival within the acidic, nitro-oxidative phagolysosome of activated macrophages.