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Tumor necrosis factor-α signaling in nonalcoholic steatohepatitis and targeted therapies

Journal of Genetics and Genomics 2022年第4期49卷 269-278页

作者： Sijia Lu Yibing Wang Junli Liu Shanghai Diabetes Institute Department of Endocrinology and MetabolismShanghai Jiao Tong University Affiliated Sixth People’s HospitalShanghai 200233China School of Kinesiology Shanghai University of SportsShanghai 200438China

Nonalcoholic steatohepatitis(NASH),an inflammatory subtype of nonalcoholic fatty liver disease,is featured by significantly elevated levels of various proinflammatory cytokines.Among numerous proinflammatory factors that contribute to NASH pathogenesis,the secreted protein,tumor necrosis factoralpha(tnf-α),plays an essential role in multiple facets of NASH progression and is therefore considered as a potential therapeutic target.In this review,we will first systematically describe the preclinical studies on the biochemical function of tnf-αand its intracellular downstream signaling mechanisms through its receptors.Moreover,we extensively discuss its functions in regulating inflammation,cell death,and fibrosis of liver cells in the pathogenesis of NASH,and the molecular mechanism that tnf-αexpression is regulated by NF-κB and other upstream master regulators during NASH progression.As tnf-αis one of the causal factors that remarkably contributes to NASH progression,combination of therapeutic modalities,including tnf-α-based therapies may lead to the resolution of NASH via multiple pathways and thus generate clinical benefits.For translational studies,we summarize recent advances in strategies targeting tnf-αand its signaling pathway,which paves the way for potential therapeutic treatments for NASH in the future.

关键词： tnf-αsignaling NASH Inflammation Cell death Fibrosis

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A shedding soluble form of interleukin-17 receptor D exacerbates collagen-induced arthritis through facilitating tnf-α-dependent receptor clustering

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Cellular & Molecular Immunology 2021年第8期18卷 1883-1895页

作者： Sihan Liu Yanxia Fu Kunrong Mei Yinan Jiang Xiaojun Sun Yinyin Wang Fangli Ren Congshan Jiang Liesu Meng Shemin Lu Zhihai Qin Chen Dong Xinquan Wang Zhijie Chang Shigao Yang State Key Laboratory of Membrane Biology School of MedicineTsinghua University100084BeijingChina The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area Shantou University Medical CollegeShantou515041GuangdongChina Department of Biochemistry and Molecular Biology Capital Medical University100069BeijingChina Center for Structural Biology School of Life SciencesMinistry of Education Key Laboratory of Protein ScienceTsinghua University100084BeijingChina Department of Biochemistry and Molecular Biology School of Basic Medical ScienceXi’an Jiaotong University Health Science CenterKey Laboratory of Environment and Genes Related to Diseases(Xi’an Jiaotong University)Ministry of EducationXi’an710061ShanxiChina Key Laboratory of Protein and Peptide Pharmaceuticals CAS-University of Tokyo Joint Laboratory of Structural Virology and ImmunologyInstitute of BiophysicsChinese Academy of Sciences100101BeijingChina Institute for Immunology and School of Medicine Tsinghua University100084BeijingChina School of Life Sciences Anhui Medical UniversityHefei230032China

Rheumatoid arthritis(RA)is exacerbated by tnf-alpha signaling.However,it remains unclear whether tnf-α-activated tnfR1 and tnfR2 are regulated by extracellular factors.Here,we showed that soluble glycosylated interleukin-17 receptor D(sIL-17RD),which was produced by proteolytic cleavage,enhanced tnf-α-induced RA.We revealed that IL-17RD shedding was induced by the proteolytic enzyme TACE and enhanced by tnf-αexpression in macrophages.Intriguingly,sIL-17RD was elevated in the sera of arthritic mice and rats.Recombinant sIL-17RD significantly enhanced the tnf-α-induced proinflammatory response by promoting tnf-α-tnfR-sIL-17RD complex formation and receptor clustering,leading to the accelerated development of collagen-induced arthritis.Our observations revealed that ectodomain shedding of IL-17RD occurred in RA to boost the tnf-α-induced inflammatory response.Targeting sIL-17RD may provide a new strategy for the therapy of RA.

关键词： IL-17RD TACE/ADAM17 Ectodomain shedding tnf-αsignaling Arthritis

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