Recent studies have implicated the miRNAs in the pathogenesis of immune system mediated pulmonary diseases. Tan and colleagues [87] described that a single nucleotide polymorphism in the 3'UTR of HLA-G, a known asthma-susceptibility gene, disrupts the binding sites of three miRNAs (miR-148a, miR-148b, miR-152) targeting this gene. Thus, it is likely that the association of the HLA-G gene to asthma-susceptibility may be due to the allele-specific regulation of this gene by miRNAs [87] . MiR-21 is a further miRNA crucially involved in allergic lung inflammation. Its molecular target is IL-12p35, a cytokine contributing to polarization of Th cells toward Th2 cells [88] . MiR-126 is another miRNA found to be involved in the pathogenesis of allergic airways disease [89] . The blockade of miR-126 suppressed the asthmatic phenotype leading to diminished Th2 responses, suppression of inflammation, reduced airways hyperresponsiveness, inhibition of eosinophil recruitment, and lower mucus hypersecretion [89] . In bronchial epithelial cells stimulated with IL-4 and TNFα, let-7, miR-29a and miR-155 have been involved in the regulation of allergic inflammation [90] . Multiple members of let-7 family were also found upregulated in experimental asthma model and the pro-inflammatory role of let-7 miRNAs on the allergic cytokine expression was confirmed [91] . Another study showed that expression of RhoA in bronchial smooth muscle cells (BSMCs), a new target for asthma therapy, is negatively regulated by miR-133a [92] . The same group later revealed that IL-13 is capable of reducing the miR-133a expression in BSMCs and that the miR-133a downregulation causes an Table 5 MiRNAs involved in pathological processes in the lung miRNA Function (A animal studies, H human studies) References miR-155, miR-17-92 cluster deregulation results in uncontrolled inflammation (A) [70] , [71] , [77] miR-21, miR-27b, miR-100, miR-181c, miR-223, miR-224 increased following exposure to LPS (A) [72] miR-155 overexpressed in solid tumors, inhibition of tumor suppressor genes (A, H) [81] miR-223 impaired granulocyte function, regulator of granulocyte production and inflammatory response (A) [82] miR-148a/b, miR-152 allele-specific regulation of asthma susceptibility HLA-G gene (H) [87] miR-21 key role in asthma (A) [88] overexpressed in solid malignancies (A, H) [103] up-regulated in bleomycin-induced fibrosis and IPF (A, H) [110] miR-126 suppression of the asthmatic phenotype by blockade of miR-126 (A) [89] downregulated in cystic fibrosis airway epithelial cells (H) [111] let-7, miR-29a, miR-155 regulation of allergic inflammation in bronchial epithelial cells (A, H) [90] let-7 pro-inflammatory effect in experimental asthma (A) [91] role in lung cancer progression (H) [99] miR-133a regulator of expression of RhoA, target for asthma therapy (A, H) [92] , [93] miR-146a reduced expression in COPD fibroblasts (H) [95] miR-218, miR-15a, miR-199b, miR-125a/b, miR-294 deregulated due to smoking (A, H) [96, 97] miR-218 tumor suppressor in non-small cell lung cancer (H) [98] miR-17-92 cluster overexpressed in lung cancers (H) [102] miR-34 regulation of apoptosis in lung cancer cells (H) [105] [106] [107] miR-210 overexpressed in lung cancer (H) [108] let-7d pro-fibrotic effect in pulmonary fibrosis (A, H) [109] upregulation of RhoA, presumably resulting in an augmentation of the contraction [93] .