The outcome of the interaction between Mycobacterium tuberculosis (Mtb) and a macrophage depends on the interplay between host defense and bacterial immune subversion mechanisms. MicroRNAs (miRNAs) critically regulate several host defense pathways, but their role in the Mtb-macrophage interplay remains unclear.
Recently, Kumar et al. performed a miRNA profiling, and investigated the downregulation of miR-let-7f in a manner dependent on the Mtb secreted effector ESAT-6.
The authors established that let-7f targets A20 (TNFAIP3), which is a feedback inhibitor of the NF-κB pathway. In parallel, the expression of let-7f decreases and A20 increases with the progression of Mtb infection in mice. The team also described that the production of TNFa and other mediators involved in immunity to Mtb, is correspondingly increased.
These results uncover a role for let-7f and its target A20 in regulating immune responses to Mtb and controlling bacterial burden.
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![IF analysis of Daudi cells with A20 /TNFAIP3 antibody [EPR2663] (cat. nr 210GTX62211red) and DAPI (blue).](http://5.196.212.231/wp-content/uploads/2099/11/GTX62211.jpg)
Kumar M. et al. “MicroRNA let-7 modulates the immune response to Mycobacterium tuberculosis infection via control of A20, an inhibitor of the NF-kB pathway” (2015) Cell Host Microbe. 11;17(3):345-56. doi: 10.1016/j.chom.2015.01.007.
