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-őļB 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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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.