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. Author manuscript; available in PMC: 2015 Dec 15.
Published in final edited form as: Adv Exp Med Biol. 2013;783:103–120. doi: 10.1007/978-1-4614-6111-1_6

Figure 1. Two major pathways leading to macrophage death following M. tuberculosis infection.

Figure 1

Some macrophages death programs are triggered by the extrinsic pathway (surface receptor mediated): Ligation of death receptor (e.g. Fas or TNF-α receptors) is followed by activation of caspase-8 which leads to apoptosis. Alternatively, the Intrinsic Pathway (mitochondria-mediated) is activated: Permeabilization of mitochondria outer membrane potential (MOMP) leads to release of apoptotic mediators such as cytochrome c from the mitochondrial intermembrane space into the cytosol leading to formation of apoptosome complex and activation of caspases (9, 3, and 7) which in turn induce apoptosis. However, during necrosis mitochondrial permeability transition (MPT) causes mitochondrial inner membrane perturbation (MIMP), collapse of the membrane potential, uncoupling of the respiratory chain, and overproduction of reactive oxygen species (ROS). Cyclophilin D (CypD) is a mitochondrial protein which is involved in MPT and necrosis.