The regulatory mechanism of miRNA in response to Mycobacterium tuberculosis (MTB) infection is not clear yet. Autophagy has recently been identified as an effective way to control the intracellular MTB survival. In the present study, we demonstrate a novel role of miR-30A in negatively regulating the autophagy-mediated anti-MTB response. We found that overexpression of miR-30A could surppress the elimation of intracellular MTB, and this process was through inhibition of autophagy. Further more, there was a negatively correlation between miR-30A and beclin-1 in MTB positive patients, and miR-30A expression were refectious after anti-TB treatment. The results indicated that the miR-30A expression level plays a key role in immunity response against MTB and this might provide potential targets for the future treatment of tuberculosis infection.