The immunomodulatory role of interleukin-35 in fibrotic diseases

Fibrosis makes numerous diseases in all organs more complicated and leads to severe consequences in the lung, liver, heart, kidney, and skin. In essence, fibrosis results from excessive, persistent and oftentimes nonreversible aggregation of extracellular matrix (ECM) or simply as collagen during the process of tissue injury and repair. Recent studies suggest the pathology of fibrosis, especially in pulmonary and liver fibrosis, involves various types of immune cells and soluble mediators including interleukin (IL)-35, a recently identified heterodimeric cytokine that belongs to the IL-12 cytokine family. Furthermore, IL-35 may inhibit fibrotic diseases. However, the side effects of inhibiting IL-35 also need attention and we have a long way to go to make better use of it in fibrotic diseases. Areas covered: This review focuses on recent evidence regarding the role of IL-35 in the pathogenesis of pulmonary, hepatic, cardiac, renal and skin fibrosis. It also discusses targeting of IL-35 as a promising novel strategy for treatment of fibrotic diseases. Expert commentary: Understanding as fully as possible the relationship between IL-35 and fibrotic diseases is important for the development of new therapeutic approaches.