Mycobacterium tuberculosis controls MicroRNA-99b (miR-99b) expression in infected murine dendritic cells to modulate host immunity

Yogesh Singh; Vandana Kaul; Alka Mehra; Samit Chatterjee; Sultan Tousif; Ved Prakash Dwivedi; Mrutyunjay Suar; Luc Van Kaer; William R. Bishai; Gobardhan Das

doi:10.1074/jbc.C112.439778

Mycobacterium tuberculosis controls MicroRNA-99b (miR-99b) expression in infected murine dendritic cells to modulate host immunity

Yogesh Singh, Vandana Kaul, Alka Mehra, Samit Chatterjee, Sultan Tousif, Ved Prakash Dwivedi, Mrutyunjay Suar, Luc Van Kaer, William R. Bishai, Gobardhan Das

Research output: Contribution to journal › Article › peer-review

142 Scopus citations

Abstract

Background: Modulation of host miRNAs coincides with increased pathogenicity in various infectious diseases. Results: miR-99b is up-regulated in M. tuberculosis-infected dendritic cells, which inhibits production of proinflammatory cytokines. Conclusion: Our findings unfold a novel immune evasion strategy of M. tuberculosis by modulating miRNAs. Significance: Our study opens up the possibility to design vaccines and immunotherapies for tuberculosis by targeting specific miRNAs.

Original language	English (US)
Pages (from-to)	5056-5061
Number of pages	6
Journal	Journal of Biological Chemistry
Volume	288
Issue number	7
DOIs	https://doi.org/10.1074/jbc.C112.439778
State	Published - Feb 15 2013

ASJC Scopus subject areas

Biochemistry
Molecular Biology
Cell Biology

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title = "Mycobacterium tuberculosis controls MicroRNA-99b (miR-99b) expression in infected murine dendritic cells to modulate host immunity",

abstract = "Background: Modulation of host miRNAs coincides with increased pathogenicity in various infectious diseases. Results: miR-99b is up-regulated in M. tuberculosis-infected dendritic cells, which inhibits production of proinflammatory cytokines. Conclusion: Our findings unfold a novel immune evasion strategy of M. tuberculosis by modulating miRNAs. Significance: Our study opens up the possibility to design vaccines and immunotherapies for tuberculosis by targeting specific miRNAs.",

author = "Yogesh Singh and Vandana Kaul and Alka Mehra and Samit Chatterjee and Sultan Tousif and Dwivedi, {Ved Prakash} and Mrutyunjay Suar and {Van Kaer}, Luc and Bishai, {William R.} and Gobardhan Das",

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AU - Singh, Yogesh

AU - Kaul, Vandana

AU - Mehra, Alka

AU - Chatterjee, Samit

AU - Tousif, Sultan

AU - Dwivedi, Ved Prakash

AU - Suar, Mrutyunjay

AU - Van Kaer, Luc

AU - Bishai, William R.

AU - Das, Gobardhan

PY - 2013/2/15

Y1 - 2013/2/15

N2 - Background: Modulation of host miRNAs coincides with increased pathogenicity in various infectious diseases. Results: miR-99b is up-regulated in M. tuberculosis-infected dendritic cells, which inhibits production of proinflammatory cytokines. Conclusion: Our findings unfold a novel immune evasion strategy of M. tuberculosis by modulating miRNAs. Significance: Our study opens up the possibility to design vaccines and immunotherapies for tuberculosis by targeting specific miRNAs.

AB - Background: Modulation of host miRNAs coincides with increased pathogenicity in various infectious diseases. Results: miR-99b is up-regulated in M. tuberculosis-infected dendritic cells, which inhibits production of proinflammatory cytokines. Conclusion: Our findings unfold a novel immune evasion strategy of M. tuberculosis by modulating miRNAs. Significance: Our study opens up the possibility to design vaccines and immunotherapies for tuberculosis by targeting specific miRNAs.

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Mycobacterium tuberculosis controls MicroRNA-99b (miR-99b) expression in infected murine dendritic cells to modulate host immunity

Abstract

ASJC Scopus subject areas

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