Xin Qin, Jinglin Gao, Xiuhua Liu, Jie Chen, Xinghui Song
{"title":"HMGB1对SLE小鼠免疫细胞影响的研究","authors":"Xin Qin, Jinglin Gao, Xiuhua Liu, Jie Chen, Xinghui Song","doi":"10.1016/j.bbrep.2025.102262","DOIUrl":null,"url":null,"abstract":"<div><div>Systemic lupus erythematosus (SLE) is a complex autoimmune disease, and its pathogenesis is related to the balance and dysfunction of dendritic cells (DCs). The therapy targeting dendritic cells has become an important means to treat SLE and autoimmune diseases. Besides, HMGB1 is highly expressed in the serum of patients with SLE. Therefore, this study intended to find the function of HMGB1 on immune cells in SLE. We used the MRL/lpr mice as SLE model animals, then we isolated the peripheral blood of SLE mice to obtain CD14<sup>+</sup> cells, which was induced into monocyte-derived Dendritic cells (Mo-DCs). We also obtained CD14<sup>+</sup> cells from peripheral blood to explore the effect of HMGB1 treated Mo-DCs. Then followed the HMGB1 treatment, flow cytometry, ELISA, WB and CCK8 assay. The results showed that HMGB1 can stimulate the maturation of DCs, and activated mTOR pathway, and affect the proliferation and differentiation of CD4<sup>+</sup> cells. What's more, HMGB1 seemed to enter cells through the endocytosis of Toll-like receptor, and its function maybe related to endoplasmic reticulum stress. The further research found tunicamycin (endoplasmic reticulum stress inducer) and rapamycin (mTOR inhibitor) can inhibit the activation of Mo-DCs. Therefore, we thought that HMGB1 enters DCs by TLR6 and regulate the activation of DCs and the differentiation of CD4<sup>+</sup> cells by influencing endoplasmic reticulum stress and the mTOR pathway.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"44 ","pages":"Article 102262"},"PeriodicalIF":2.2000,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Study on the effect of HMGB1 on immune cells isolated from SLE mice\",\"authors\":\"Xin Qin, Jinglin Gao, Xiuhua Liu, Jie Chen, Xinghui Song\",\"doi\":\"10.1016/j.bbrep.2025.102262\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Systemic lupus erythematosus (SLE) is a complex autoimmune disease, and its pathogenesis is related to the balance and dysfunction of dendritic cells (DCs). The therapy targeting dendritic cells has become an important means to treat SLE and autoimmune diseases. Besides, HMGB1 is highly expressed in the serum of patients with SLE. Therefore, this study intended to find the function of HMGB1 on immune cells in SLE. We used the MRL/lpr mice as SLE model animals, then we isolated the peripheral blood of SLE mice to obtain CD14<sup>+</sup> cells, which was induced into monocyte-derived Dendritic cells (Mo-DCs). We also obtained CD14<sup>+</sup> cells from peripheral blood to explore the effect of HMGB1 treated Mo-DCs. Then followed the HMGB1 treatment, flow cytometry, ELISA, WB and CCK8 assay. The results showed that HMGB1 can stimulate the maturation of DCs, and activated mTOR pathway, and affect the proliferation and differentiation of CD4<sup>+</sup> cells. What's more, HMGB1 seemed to enter cells through the endocytosis of Toll-like receptor, and its function maybe related to endoplasmic reticulum stress. The further research found tunicamycin (endoplasmic reticulum stress inducer) and rapamycin (mTOR inhibitor) can inhibit the activation of Mo-DCs. Therefore, we thought that HMGB1 enters DCs by TLR6 and regulate the activation of DCs and the differentiation of CD4<sup>+</sup> cells by influencing endoplasmic reticulum stress and the mTOR pathway.</div></div>\",\"PeriodicalId\":8771,\"journal\":{\"name\":\"Biochemistry and Biophysics Reports\",\"volume\":\"44 \",\"pages\":\"Article 102262\"},\"PeriodicalIF\":2.2000,\"publicationDate\":\"2025-09-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biochemistry and Biophysics Reports\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2405580825003498\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochemistry and Biophysics Reports","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2405580825003498","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Study on the effect of HMGB1 on immune cells isolated from SLE mice
Systemic lupus erythematosus (SLE) is a complex autoimmune disease, and its pathogenesis is related to the balance and dysfunction of dendritic cells (DCs). The therapy targeting dendritic cells has become an important means to treat SLE and autoimmune diseases. Besides, HMGB1 is highly expressed in the serum of patients with SLE. Therefore, this study intended to find the function of HMGB1 on immune cells in SLE. We used the MRL/lpr mice as SLE model animals, then we isolated the peripheral blood of SLE mice to obtain CD14+ cells, which was induced into monocyte-derived Dendritic cells (Mo-DCs). We also obtained CD14+ cells from peripheral blood to explore the effect of HMGB1 treated Mo-DCs. Then followed the HMGB1 treatment, flow cytometry, ELISA, WB and CCK8 assay. The results showed that HMGB1 can stimulate the maturation of DCs, and activated mTOR pathway, and affect the proliferation and differentiation of CD4+ cells. What's more, HMGB1 seemed to enter cells through the endocytosis of Toll-like receptor, and its function maybe related to endoplasmic reticulum stress. The further research found tunicamycin (endoplasmic reticulum stress inducer) and rapamycin (mTOR inhibitor) can inhibit the activation of Mo-DCs. Therefore, we thought that HMGB1 enters DCs by TLR6 and regulate the activation of DCs and the differentiation of CD4+ cells by influencing endoplasmic reticulum stress and the mTOR pathway.
期刊介绍:
Open access, online only, peer-reviewed international journal in the Life Sciences, established in 2014 Biochemistry and Biophysics Reports (BB Reports) publishes original research in all aspects of Biochemistry, Biophysics and related areas like Molecular and Cell Biology. BB Reports welcomes solid though more preliminary, descriptive and small scale results if they have the potential to stimulate and/or contribute to future research, leading to new insights or hypothesis. Primary criteria for acceptance is that the work is original, scientifically and technically sound and provides valuable knowledge to life sciences research. We strongly believe all results deserve to be published and documented for the advancement of science. BB Reports specifically appreciates receiving reports on: Negative results, Replication studies, Reanalysis of previous datasets.