Mycobacterium tuberculosis Inhibits Neutrophil Apoptosis, Leading to Delayed Activation of Naive CD4 T cells
Cell Host & Microbe, ISSN: 1931-3128, Vol: 11, Issue: 1, Page: 81-90
2012
- 153Citations
- 234Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations153
- Citation Indexes153
- 153
- CrossRef132
- Captures234
- Readers234
- 234
Article Description
Mycobacterium tuberculosis promotes its replication by inhibiting the apoptosis of infected macrophages. A proapoptotic M. tuberculosis mutant lacking nuoG, a subunit of the type I NADH dehydrogenase complex, exhibits attenuated growth in vivo, indicating that this virulence mechanism is essential. We show that M. tuberculosis also suppresses neutrophil apoptosis. Compared to wild-type, the nuoG mutant spread to a larger number of lung phagocytic cells. Consistent with the shorter lifespan of infected neutrophils, infection with the nuoG mutant resulted in fewer bacteria per infected neutrophil, accelerated bacterial acquisition by dendritic cells, earlier trafficking of these dendritic cells to lymph nodes, and faster CD4 T cell priming. Neutrophil depletion abrogated accelerated CD4 T cell priming by the nuoG mutant, suggesting that inhibiting neutrophil apoptosis delays adaptive immunity in tuberculosis. Thus, pathogen modulation of apoptosis is beneficial at multiple levels, and enhancing phagocyte apoptosis promotes CD4 as well as CD8 T cell responses.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1931312811004045; http://dx.doi.org/10.1016/j.chom.2011.11.012; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84856003520&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/22264515; https://facultyopinions.com/prime/13697956#eval15112056; http://dx.doi.org/10.3410/f.13697956.15112056; https://linkinghub.elsevier.com/retrieve/pii/S1931312811004045; https://facultyopinions.com/prime/13697956#eval15478096; http://dx.doi.org/10.3410/f.13697956.15478096; http://www.cell.com/cell-host-microbe/abstract/S1931-3128(11)00404-5?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1931312811004045%3Fshowall%3Dtrue; http://linkinghub.elsevier.com/retrieve/pii/S1931312811004045; http://f1000.com/13697956#eval15112056; http://f1000.com/13697956#eval15478096
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