IL1B and tuberculosis: For instance, hsa-mir-146a-5p is a well-known regulator of innate immune activation pathway by inhibiting toll-like receptor and NF-κB signalling (41); while hsa-mir-223-3p, which was differentially expressed in our study, has been shown to negatively regulate excessive innate immune responses by controlling myeloid cells and macrophages activation; and NLRP3 inflammasome activity, thereby modulating IL-1β production (38), that is a reported cytokine significantly implicated in the aberrant inflammation associated with TB-IRIS (15).