Autophagy Meets Phagocytosis

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Autophagy Meets Phagocytosis Ken Cadwell, Jennifer A. Philips Immunity Volume 39, Issue 3, Pages 425-427 (September 2013) DOI: 10.1016/j.immuni.2013.08.027 Copyright © 2013 Elsevier Inc. Terms and Conditions

Figure 1 Autophagy Inhibits Internalization and Intracellular Survival of Mycobacterium tuberculosis After phagocytosis by macrophages, M. tuberculosis (Mtb) bacilli that escape into the cytosol or remain in a damaged vacuole can be recognized by the adaptor protein p62 and targeted for degradation in the autolysosome (autophagosome fused with lysosome). p62 also brings antimicrobial precursor molecules derived from ubiquitin and ribosomal proteins to the autolysosome for processing. In an autophagy-deficient cell, these antimicrobial processes are disrupted, and this innate immune defect is exacerbated by p62 accumulation. Excess p62 binds KEAP1 and releases Nrf2, which is then able to translocate to the nucleus and increase scavenger receptor expression. Because Mtb uses scavenger receptors for internalization, autophagy-deficient macrophages display enhanced Mtb uptake, and the increase in intracellular bacteria cannot be resolved. Immunity 2013 39, 425-427DOI: (10.1016/j.immuni.2013.08.027) Copyright © 2013 Elsevier Inc. Terms and Conditions