The IL-1 family, whose biological properties are typically pro-inflammatory and pro-fibrosis, has been associated with systemic sclerosis (SSc). For example, Expression of IL-1α and IL-1β was enhanced in SSc fibroblasts. IL-33 could increase IL-13 expression in mononuclear and eosinophil, and IL-13 might promote IL-33-induced cutaneous fibrosis by increasing collagen VI, collagen III, and MMP-1. In recent years, four new members (IL-36α, β, γ, and IL-37) have been identified and expanded the IL-1 family. These cytokines are implicated in the pathogenesis of various autoimmune diseases, but their role in the regulation of extracellular matrix expression and its contribution to the phenotype of SSc remain to be elucidated. Up to now, we have extensively studied the involvement of novel cytokines on skin fibrosis using experimental systems of cultured fibroblasts. We discovered that IL-17, IL-20, IL-23 and IL-35 are involved in the expression of type I collagen. In this study, we also conducted experiments on new IL-1 family cytokines in a similar manner and find out that IL-37 enhanced the expression of type I collagen. IL-37 is thought to be a cytokine that suppresses innate immunity, but it is unclear whether it binds to IL-18Rα and exerts its function in vivo. Clarifying the mechanism regulating the extracellular matrix expression by IL-37 in SSc skin may lead to better understanding of this disease and new therapeutic strategies.