TY - JOUR T1 - New IL-1 family IL-38 is highly expressed in alveolar cells of drug-induced lung injury and idiopathic pulmonary fibrosis JF - European Respiratory Journal JO - Eur Respir J DO - 10.1183/13993003.congress-2016.PA3088 VL - 48 IS - suppl 60 SP - PA3088 AU - Masaki Tominaga AU - Masaki Okamoto AU - Takashi Kinoshita AU - Yuki Sakazaki AU - Masanobu Matsuoka AU - Shinjiro Kaieda AU - Tomoaki Hoshino Y1 - 2016/09/01 UR - http://erj.ersjournals.com/content/48/suppl_60/PA3088.abstract N2 - Objectives: The newly characterized cytokine IL-38 is a member of the IL-1 family but its action remains unknown. In order to clarify the function of IL-38, we examined its immunohistochemical expression in several types of interstitial lung disease (ILD).Methods: We generated an anti-human IL-38 monoclonal antibody (clone H127C) and used it to immunohistochemically examine the expression of IL-38 protein in lung tissues obtained from 12 patients with idiopathic pulmonary fibrosis/usual interstitial pneumonia (IPF/UIP), 5 with acute exacerbation of IPF, 10 with drug-induced ILD, and 22 control subjects.Results: IL-38 protein was not strongly expressed in pulmonary alveolar tissues in all of the 22 control subjects. In contrast, IL-38 was overexpressed in the lungs of 4/5 (80%) patients with acute exacerbation of IPF and all (10/10, 100%) of the patients with drug-induced ILD. It was noteworthy that IL-38 overexpression was limited to hyperplastic type II pneumocytes, which are considered to reflect regenerative change following diffuse alveolar damage in ILD.Conclusions: Our present findings indicate that IL-38 protein is overexpressed in areas of local inflammation in some forms of acute lung injury such as drug-induced ILD and acute exacerbation of IPF. IL-38 may regulate the process of regeneration and acute and/or chronic deterioration in ILDs. ER -