Unique role for ATG5 in neutrophil-mediated immunopathology during M. tuberculosis infection
Jacqueline M. Kimmey,
Jeremy P. Huynh,
Leslie A. Weiss,
Sunmin Park,
Amal Kambal,
Jayanta Debnath,
Herbert W. Virgin and
Christina L. Stallings ()
Additional contact information
Jacqueline M. Kimmey: Washington University School of Medicine
Jeremy P. Huynh: Washington University School of Medicine
Leslie A. Weiss: Washington University School of Medicine
Sunmin Park: Washington University School of Medicine
Amal Kambal: Washington University School of Medicine
Jayanta Debnath: University of California, San Francisco
Herbert W. Virgin: Washington University School of Medicine
Christina L. Stallings: Washington University School of Medicine
Nature, 2015, vol. 528, issue 7583, 565-569
Abstract:
Genetic engineering in mice reveals that autophagy is not an essential mechanism in myeloid cells for controlling Mycobacterium tuberculosis infection, and that autophagy factor ATG5 protects organisms by regulating neutrophil influx and tissue damage.
Date: 2015
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DOI: 10.1038/nature16451
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