TY - JOUR
T1 - Roles of IL-1 and IL-10 family cytokines in the progression of systemic lupus erythematosus
T2 - Friends or foes?
AU - Wu, Yi Rou
AU - Hsing, Chung Hsi
AU - Chiu, Chiao Juno
AU - Huang, Hsin Yi
AU - Hsu, Yu Hsiang
N1 - Funding Information:
This work was supported by the Ministry of Science and Technology of Taiwan (MOST‐108‐2321‐B‐002‐057‐MY3, MOST‐109‐2628‐B‐006‐019, and MOST‐110‐2628‐B‐006‐023).
Publisher Copyright:
© 2021 International Union of Biochemistry and Molecular Biology.
PY - 2022/2
Y1 - 2022/2
N2 - 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.
AB - 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.
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U2 - 10.1002/iub.2568
DO - 10.1002/iub.2568
M3 - Article
C2 - 34668305
AN - SCOPUS:85117173043
VL - 74
SP - 143
EP - 156
JO - Biochemistry and Molecular Biology International
JF - Biochemistry and Molecular Biology International
SN - 1521-6543
IS - 2
ER -