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Tuberculosis

Autophagy is not the answer

Nature volume 528, pages 482–483 (2015)Cite this article

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The cellular process of autophagy has been proposed to help kill Mycobacterium tuberculosis. But although the autophagy gene Atg5 is key to host immunity, other autophagy genes do not affect the outcome of tuberculosis. See Letter p.565

More people die each year from tuberculosis than from any other infectious disease. The bacterium Mycobacterium tuberculosis is transmitted between people by aerosol droplets generated by someone with active lung disease. The immune response prevents disease in most infected people, but the bacteria often persist as an asymptomatic (latent) infection. Many studies have found that the process of autophagy, through which cellular components are broken down and recycled, contributes to the killing of M. tuberculosis. In this issue, Kimmey et al.1 (page 565) present evidence supporting the previous finding that the autophagy gene Atg5 plays a key part in the host response to M. tuberculosis infection, but they show that loss of many other autophagy genes does not significantly influence disease outcome. These results suggest that Atg5 is essential for restricting M. tuberculosis growth, but that the conventional autophagy pathway is not.

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Figure 1: Defence against Mycobacterium.

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Authors and Affiliations

  1. Samuel M. Behar is in the Department of Microbiology and Physiological Systems, and Eric H. Baehrecke is in the Department of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.,

    Samuel M. Behar & Eric H. Baehrecke

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  1. Samuel M. Behar
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  2. Eric H. Baehrecke
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Correspondence to Samuel M. Behar or Eric H. Baehrecke.

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Behar, S., Baehrecke, E. Autophagy is not the answer. Nature 528, 482–483 (2015). https://doi.org/10.1038/nature16324

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