In conclusion, our findings identify a novel molecular mechanism whereby the activation of AIM2 could lead to the activation of the non-canonical inflammasome (caspase-4 dependent) that induces the release of IL-1α responsible for the release of TGF-β from PBMCs of IPF patients.
We assume from our data that the gene polymorphisms of the promotor region of IL-4 at position (-1098) and (-33) and IL-1 alpha at position (-889) are likely to play a pathogenic role in IPF and in modification of its clinical presentation and severity.
IL-1 inhibitory activities decreased in healthy smokers (HS), and patients with sarcoidosis (Sar), or idiopathic pulmonary fibrosis (IPF), compared with those in healthy nonsmokers (HNS), though an increase in IL-1 beta release was not detected.