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论文题目: Cutting Edge: Ubiquitin-Specific Protease 4 Promotes Th17 Cell Function under Inflammation by Deubiquitinating and Stabilizing ROR gamma t
英文论文题目: Cutting Edge: Ubiquitin-Specific Protease 4 Promotes Th17 Cell Function under Inflammation by Deubiquitinating and Stabilizing ROR gamma t
第一作者: Yang, J; Xu, P; Han, L; Guo, ZX; Wang, XW; Chen, ZJ; Nie, J; Yin, SY; Piccioni, M; Tsun, A; Lv, L; Ge, SL; Li, B
英文第一作者: Yang, J; Xu, P; Han, L; Guo, ZX; Wang, XW; Chen, ZJ; Nie, J; Yin, SY; Piccioni, M; Tsun, A; Lv, L; Ge, SL; Li, B
联系作者: Lv, L (reprint author), Fudan Univ, Div Rheumatol, Huashan Hosp, 12 Wulumuqi Zhong Rd, Shanghai 200040, Peoples R China.
英文联系作者: Lv, L (reprint author), Fudan Univ, Div Rheumatol, Huashan Hosp, 12 Wulumuqi Zhong Rd, Shanghai 200040, Peoples R China.
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发表年度: 2015
卷: 194
期: 9
页码: 4094-4097
摘要: ROR gamma t is a key transcription factor that controls the development and function of inflammatory Th17. The mechanisms that regulate RORgt stability remain unclear. We report that Th17 cells highly express the deubiquitinase ubiquitin-specific protease (USP) 4, which is essential for maintaining RORgt and Th17 cell function. Inhibition of the catalytic activity of USP4 with vialinin A, a compound derived from Chinese traditional medicine, dampened Th17 differentiation. USP4 interacted and deubiquitinated K48-linked polyubiquitination of RORgt, thereby promoting ROR gamma t function and IL-17A transcription. Interestingly, TGF-beta plus IL-6 enhanced USP4-mediated deubiquitination of ROR gamma t. Moreover, USP4 and IL-17 mRNA, but not RORgt mRNA, were significantly elevated in CD4(+) T cells from patients with rheumatic heart disease. Thus, USP4 could be a novel therapeutic target for the treatment of Th17-modulated autoimmune diseases.
英文摘要: ROR gamma t is a key transcription factor that controls the development and function of inflammatory Th17. The mechanisms that regulate RORgt stability remain unclear. We report that Th17 cells highly express the deubiquitinase ubiquitin-specific protease (USP) 4, which is essential for maintaining RORgt and Th17 cell function. Inhibition of the catalytic activity of USP4 with vialinin A, a compound derived from Chinese traditional medicine, dampened Th17 differentiation. USP4 interacted and deubiquitinated K48-linked polyubiquitination of RORgt, thereby promoting ROR gamma t function and IL-17A transcription. Interestingly, TGF-beta plus IL-6 enhanced USP4-mediated deubiquitination of ROR gamma t. Moreover, USP4 and IL-17 mRNA, but not RORgt mRNA, were significantly elevated in CD4(+) T cells from patients with rheumatic heart disease. Thus, USP4 could be a novel therapeutic target for the treatment of Th17-modulated autoimmune diseases.
刊物名称: JOURNAL OF IMMUNOLOGY
英文刊物名称: JOURNAL OF IMMUNOLOGY
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学科: Immunology
英文学科: Immunology
影响因子: 4.922
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论文类别: Article
英文论文类别: Article
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