interleukin (iL)-12 family member is a heterodimer glycoprotein, composed of two covalently linked subunits, α and β chains. The α subunit consists of iL-23p19, iL-27p28, and iL-12p35, and the β subunit includes iL-12p40 and epstein-Barr virus-induced gene (ebi3). iL-39 is a new heterodimeric iL-12 family member composed of iL-23p19 and ebi3 subunits. iL-39 is secreted by lipopolysaccharide-stimulated B cells. other immune cells, such as dendritic cells and macrophages, express iL-39 mRna. in lupus-like mice, gL7 + B cells and cD138 + plasma cells are highly activated and widely expressed, promoting high expression of iL-39. iL-39 mediates inflammatory responses through binding to a heterodimer of iL-23R/gp130 receptor and activation of signal transducer and activator of transcription (STaT)1/STaT3 signal molecules. The serum levels of iL-39 were significantly increased in patients with acute coronary syndrome compared with patients with normal coronary arteries. This review discusses the biological characteristics, receptor, and signal pathway as well as biological activity of iL-39 and its potential role in inflammation and other diseases.

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Pulmonary fibrosis is a disease with chronic inflammation and excessive collagen deposition for which there is no effective treatments. Interleukin (IL)-37 is a newly identified anti-inflammatory cytokine but its role in pulmonary fibrosis remains unclear. In this study, we investigated the effect of IL-37 on bleomycin-induced pulmonary fibrosis in mice. A lentivirus expressing IL-37 was administered intranasally to bleomycin-induced C57BL/6 mice. We found that IL-37 improved the survival of mice and reduced the body weight loss of mice caused by bleomycin. Furthermore, IL-37 significantly attenuated pulmonary inflammatory infiltration and collagen deposition and decreased the hydroxyproline content in bleomycin-treated mice. Finally, IL-37 treatment inhibited the expression of monocyte chemoattractant protein-1, IL-6, and tumor necrosis factor-α, but increased the expression of interferon-γ in lung tissues from bleomycin-challenged mice. Taken together, these results suggest that in vivo expression of IL-37 is useful in preventing pulmonary fibrosis induced by bleomycin and provides a possible therapeutic approach to pulmonary fibrosis diseases.

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