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Unique role for ATG5 in neutrophil-mediated immunopathology during M. tuberculosis infection

Author

Listed:
  • 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)

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.

Suggested Citation

  • Jacqueline M. Kimmey & Jeremy P. Huynh & Leslie A. Weiss & Sunmin Park & Amal Kambal & Jayanta Debnath & Herbert W. Virgin & Christina L. Stallings, 2015. "Unique role for ATG5 in neutrophil-mediated immunopathology during M. tuberculosis infection," Nature, Nature, vol. 528(7583), pages 565-569, December.
    • Handle: RePEc:nat:nature:v:528:y:2015:i:7583:d:10.1038_nature16451
    DOI: 10.1038/nature16451
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    Cited by:

    1. Tae Gun Kang & Kee Woong Kwon & Kyungsoo Kim & Insuk Lee & Myeong Joon Kim & Sang-Jun Ha & Sung Jae Shin, 2022. "Viral coinfection promotes tuberculosis immunopathogenesis by type I IFN signaling-dependent impediment of Th1 cell pulmonary influx," Nature Communications, Nature, vol. 13(1), pages 1-19, December.
    2. Ana Teresa López-Jiménez & Serge Mostowy, 2021. "Emerging technologies and infection models in cellular microbiology," Nature Communications, Nature, vol. 12(1), pages 1-13, December.

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