CD4 <sup>+</sup> T-cell–independent mechanisms suppress reactivation of latent tuberculosis in a macaque model of HIV coinfection
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- Taylor W. Foreman
- Tulane National Primate Research Center, Covington, LA 70471;
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- Smriti Mehra
- Tulane National Primate Research Center, Covington, LA 70471;
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- Denae N. LoBato
- Tulane National Primate Research Center, Covington, LA 70471;
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- Adel Malek
- Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461;
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- Xavier Alvarez
- Tulane National Primate Research Center, Covington, LA 70471;
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- Nadia A. Golden
- Tulane National Primate Research Center, Covington, LA 70471;
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- Allison N. Bucşan
- Tulane National Primate Research Center, Covington, LA 70471;
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- Peter J. Didier
- Tulane National Primate Research Center, Covington, LA 70471;
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- Lara A. Doyle-Meyers
- Tulane National Primate Research Center, Covington, LA 70471;
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- Kasi E. Russell-Lodrigue
- Tulane National Primate Research Center, Covington, LA 70471;
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- Chad J. Roy
- Tulane National Primate Research Center, Covington, LA 70471;
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- James Blanchard
- Tulane National Primate Research Center, Covington, LA 70471;
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- Marcelo J. Kuroda
- Tulane National Primate Research Center, Covington, LA 70471;
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- Andrew A. Lackner
- Tulane National Primate Research Center, Covington, LA 70471;
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- John Chan
- Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461;
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- Shabaana A. Khader
- Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110;
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- William R. Jacobs
- Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461;
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- Deepak Kaushal
- Tulane National Primate Research Center, Covington, LA 70471;
書誌事項
- 公開日
- 2016-09-06
- 権利情報
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- http://www.pnas.org/site/misc/userlicense.xhtml
- DOI
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- 10.1073/pnas.1611987113
- 公開者
- National Academy of Sciences
この論文をさがす
説明
<jats:title>Significance</jats:title> <jats:p> According to the World Health Organization, one in three humans is latently infected with <jats:italic>Mycobacterium tuberculosis</jats:italic> and 10% of these individuals risk developing active, clinical tuberculosis (TB) over their lifetimes. Coinfection with human immunodeficiency virus increases this risk substantially, with depletion of CD4 <jats:sup>+</jats:sup> T cells believed to drive disease progression. Although a minority of coinfected individuals can control the infection, the mechanisms underlying this phenomenon remain unknown. Modeling coinfection using macaques, we discovered that one-third of the animals maintained latency despite complete ablation of lung CD4 <jats:sup>+</jats:sup> T cells. We report that protective immune responses mediated by CD8 <jats:sup>+</jats:sup> T cells and B cells correlate with TB control. These findings have important implications in development of both prophylactic and therapeutic measures against TB and acquired immunodeficiency syndrome. </jats:p>
収録刊行物
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- Proceedings of the National Academy of Sciences
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Proceedings of the National Academy of Sciences 113 (38), E5636-, 2016-09-06
National Academy of Sciences
