Quantitative PCR analysis showed an increased Il12 p35 mRNA level in miR 21 chemical transfected BMDCs, while Il12 p40 wasn’t inspired. Regularly, miR 21 mimics further reduced IL 12p70 protein level and Il12 p35 mRNA expression. We then infected BMDCs in vitro by BCG, and examined the expression of endogenous IL 12 and miR 21 mRNA expression at different time points. Both IL 1-2 mRNA and miR 21 were upregulated subsequent infection. But, IL 12 transcription increased tens of folds only 1 h after infection, reaching its peak between 4 and 6 h, while miR 21 increased gradually and only slightly following infection, and this increase became more substantial after 6 h. General, miR Icotinib 21 was negatively correlated with IL 12p35 mRNA term, indicating posttranscriptional regulation of Il12p35 by miR 21. We also examined the expression of TNF, IL 6, IL 1b and IL 10 secretion in miR 21 inhibitor transfected BMDCs and in contrast to control transfected BMDCs, as recent studies suggested for a protective function of TNF, IL 6 and IL 1b in host resistance to Mtb infection, while IL 10 mostly suppresses anti mycobacterial responses. We noticed somewhat IL 6, increased expression of TNF and IL 1b in BMDCs inhibited of miR 21. Cholangiocarcinoma However, no significant alteration was observed in IL 10 expression. But when these BMDCs were co cultured with antigen specific T cells, somewhat improved IL 10 production was seen. Reports also suggested that mycobacteria illness may cause IFN c production in DCs by targeting TLRs, which may function in a autocrine manner to prime DCs them-selves. While STAT4 and IL 12 are proposed to lead to inducing IFN c in DCs, but, the IFN c expression by BMDCs was certainly low and showed no big difference after miR 21 inhibition. Via a search using TargetScan and PicTar, we found that the 30UTR of Il12p35 mRNA contains the miR 21 binding web sites that are very conserved in mammals. Moreover, Il1b mRNA, Tnf, Il6 and Il12p40 weren’t specifically within the predicted miR 21 goals, indicating for Capecitabine structure other elements involved in miR 21 mediated reduction of the cytokines. To look at the likelihood that IL 12 is controlled post transcriptionally by miR 21, a combined luciferase reporter assay was used. Luciferase phrase substantially decreased when the reporter plasmid containing the Il12p35 30UTR was co transfected with miR 21 mimics. More over, this decrease was abrogated by transfection of a containing a three base mutation in the miR 21 binding site. miR 21 also notably suppressed luciferase activity in BMDCs, even after exciting of BCG. These data show that miR 21 can inhibit IL 12 production by directly targeting the 30UTR of Il12p35 mRNA. The aforementioned results suggested that miR 21 can downregulate IL12 in addition to TNF and IL 6.