K33 only mutant ubiquitin augments bone marrow-derived dendritic cell-mediated CTL priming via PI3K-Akt pathway

IF 4.9 3区 医学 Q2 IMMUNOLOGY Immunology Pub Date : 2024-03-28 DOI:10.1111/imm.13787
Yi Yun Liang, Xiao Yan Liao, Jun Jun Jia, Yi Zhen Yin, Yue Hua Zhang, Feng Guang Gao
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Abstract

To explore the effect of K33 only mutant ubiquitin (K33O) on bone marrow-derived dendritic cells' (BMDCs') maturity, antigen uptake capability, surface molecule expressions and BMDC-mediated CTL priming, and further investigate the role of PI3K-Akt engaged in K33O-increased BMDC maturation, antigen uptake and presentation, surface molecule expressions and BMDC-based CTL priming. BMDCs were conferred K33O and other ubiquitin mutants (K33R, K48R, K63R-mutant ubiquitin) incubation or LY294002 and wortmannin pretreatment. PI3K-Akt phosphorylation, antigen uptake, antigenic presentation and CD86/MHC class I expression in BMDC were determined by western blot or flow cytometry. BMDC-based CTL proliferation and priming were determined by in vitro mixed lymphocyte reaction (MLR), ex vivo enzyme-linked immunospot assay (Elispot) and flow cytometry with intracellular staining, respectively. The treatment with K33O effectively augmented PI3K-Akt phosphorylation, BMDCs' antigen uptake, antigenic presentation, CD86/MHC class I and CD11c expressions. MLR, Elispot and flow cytometry revealed that K33O treatment obviously enhanced CTL proliferation, CTL priming and perforin/granzyme B expression. The pretreatment with PI3K-Akt inhibitors efficiently abrogated K33O's effects on BMDC. The replenishment of K33 only mutant ubiquitin augments BMDC-mediated CTL priming in bone marrow-derived dendritic cells via PI3K-Akt signalling.

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只有 K33 突变的泛素能通过 PI3K-Akt 通路增强骨髓树突状细胞介导的 CTL 引物。
目的探索仅K33突变泛素(K33O)对骨髓来源树突状细胞(BMDCs)成熟度、抗原摄取能力、表面分子表达和BMDC介导的CTL引物的影响,并进一步研究PI3K-Akt在K33O增加的BMDC成熟度、抗原摄取和呈递、表面分子表达和基于BMDC的CTL引物中的作用。将 K33O 和其他泛素突变体(K33R、K48R、K63R 突变泛素)孵育或 LY294002 和 wortmannin 预处理 BMDC。BMDC 中的 PI3K-Akt 磷酸化、抗原摄取、抗原递呈和 CD86/MHC I 类表达均通过 Western 印迹或流式细胞术进行测定。体外混合淋巴细胞反应(MLR)、体外酶联免疫吸附试验(Elispot)和带细胞内染色的流式细胞术分别测定了以 BMDC 为基础的 CTL 增殖和引物。K33O能有效增强PI3K-Akt磷酸化、BMDCs的抗原摄取、抗原呈递、CD86/MHC I类和CD11c的表达。MLR、Elispot和流式细胞术显示,K33O能明显增强CTL的增殖、CTL的启动和穿孔素/粒酶B的表达。用 PI3K-Akt 抑制剂预处理可有效减弱 K33O 对 BMDC 的影响。补充 K33 唯一突变的泛素可通过 PI3K-Akt 信号增强骨髓树突状细胞中 BMDC 介导的 CTL 诱导。
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来源期刊
Immunology
Immunology 医学-免疫学
CiteScore
11.90
自引率
1.60%
发文量
175
审稿时长
4-8 weeks
期刊介绍: Immunology is one of the longest-established immunology journals and is recognised as one of the leading journals in its field. We have global representation in authors, editors and reviewers. Immunology publishes papers describing original findings in all areas of cellular and molecular immunology. High-quality original articles describing mechanistic insights into fundamental aspects of the immune system are welcome. Topics of interest to the journal include: immune cell development, cancer immunology, systems immunology/omics and informatics, inflammation, immunometabolism, immunology of infection, microbiota and immunity, mucosal immunology, and neuroimmunology. The journal also publishes commissioned review articles on subjects of topical interest to immunologists, and commissions in-depth review series: themed sets of review articles which take a 360° view of select topics at the heart of immunological research.
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