한빛사논문
- 조회551
Jae-Sung Kim 1,2, Hyo Keun Kim 3,4, Joongho Lee 5, Sein Jang 3,4, Euni Cho 1,4, Seok-Jun Mun 1,4, Seokhyun Yoon 6, Chul-Su Yang 3,4
1Department of Bionano Technology, Hanyang University, Seoul, 04673, Korea.
2Institute of Natural Science & Technology, Hanyang University, Ansan, 15588, Korea.
3Department of Molecular and Life Science, Hanyang University, Ansan, 15588, Korea.
4Center for Bionano Intelligence Education and Research, Ansan, 15588, Korea.
5Department of Computer Science, College of SW Convergence, Dankook University, Yongin, 16890, Korea.
6Department of Electronics & Electrical Engineering, College of Engineering, Dankook University, Yongin, 16890, Korea.
Corresponding author : Correspondence to Chul-Su Yang.
Abstract
CD82 is a transmembrane protein that is involved in cancer suppression and activates immune cells; however, information on the NLRP3 inflammasome is limited. Herein, we show that although CD82 suppressed the activation of the NLRP3 inflammasome in vivo and in vitro, CD82 deficiency decreased the severity of colitis in mice. Furthermore, two binding partners of CD82, NLRP3 and BRCC3, were identified. CD82 binding to these partners increased the degradation of NLRP3 by blocking BRCC3-dependent K63-specific deubiquitination. Previous studies have shown that CD82-specific bacteria in the colon microbiota called Bacteroides vulgatus (B. vulgatus) regulated the expression of CD82 and promoted the activation of the NLRP3 inflammasome. Accordingly, we observed that B. vulgatus administration increased mouse survival by mediating CD82 expression and activating NLRP3 in mice with colitis. Overall, this study showed that CD82 suppression reduced the pathogenesis of colitis by elevating the activation of the NLRP3 inflammasome through BRCC3-dependent K63 deubiquitination. Based on our findings, we propose that B. vulgatus is a novel therapeutic candidate for colitis.
논문정보
- Research article
- 2023년 02월 (BRIC 등록일 2023-02-16)
- 국내 연구진
- 생명과학 > 감염생물학
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