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. 2015 Feb 21;15:39. doi: 10.1186/s12866-015-0366-z

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© Bai et al.; licensee BioMed Central. 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Cell death pathways hypothesized to be involved in IL-32 control of MTB infection in macrophages. Macrophages can undergo apoptosis through various mechanisms including those mediated by caspase-3, caspase-1, cathepsins, and AIF. While all four pathways contribute to macrophage control of MTB infection, caspase-3, caspase-1, and cathepsins, but not AIF, mediate the anti-MTB effects of IL-32γ in macrophages. Fragmented DNA is used to depict the various forms of programmed cell death. Both extrinsic and intrinsic pathways of classical apoptosis are shown in the caspase-3-dependent apoptosis. MTB are illustrated by red bacilli in phagosomes.