Roles of IL-1 and IL-10 family cytokines in the progression of systemic lupus erythematosus: Friends or foes?

Yi Rou Wu, Chung Hsi Hsing, Chiao Juno Chiu, Hsin Yi Huang, Yu Hsiang Hsu

研究成果: Article同行評審

19 引文 斯高帕斯(Scopus)


Systemic lupus erythematosus (SLE) is a chronic autoimmune disease of unknown etiology that can affect nearly every organ system in the body. Besides genetic and environmental factors, unbalanced pro-inflammatory and anti-inflammatory cytokines contribute to immune dysregulation, trigger an inflammatory response, and induce tissue and organ damage. Inflammatory responses in SLE can be promoted and/or maintained by the availability of cytokines that are overproduced systemically and/or in local tissues. Several key cytokines have been considered potential targets for the reduction of chronic inflammation in SLE. Recent studies indicated that dysregulated production of several cytokines, including those of the IL-1 family and IL-10 family, orchestrate immune activation and self-tolerance, play critical roles in the pathogenesis of SLE. Among IL-1 family cytokines, IL-1, IL-18, IL-33, IL-36, IL-37, and IL-38 had been the most thoroughly investigated in SLE. Additionally, IL-10 family cytokines, IL-10, IL-20, IL-22, IL-26, IL-28, and IL-29 are dysregulated in SLE. Therefore, a better understanding of the initiation and progression of SLE may provide suitable novel targets for therapeutic intervention. In this review, we discuss the involvement of inflammation in the pathogenesis of SLE, with a focus on IL-1 family and IL-10 family cytokines, and highlight pathophysiological approaches and therapeutic potential for treating SLE.

頁(從 - 到)143-156
期刊IUBMB Life
出版狀態Published - 2022 2月

All Science Journal Classification (ASJC) codes

  • 生物化學
  • 分子生物學
  • 遺傳學
  • 臨床生物化學
  • 細胞生物學


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