M2巨噬细胞促进IL-10+ b细胞生成,减轻小鼠哮喘。

IF 4.1 Q2 IMMUNOLOGY
Immunotherapy advances Pub Date : 2025-03-10 eCollection Date: 2025-01-01 DOI:10.1093/immadv/ltaf007
Baichao Yu, Xueqi Wang, Yongkun Zheng, Wenjun Wang, Xiaoqin Cheng, Yue Cao, Mingxing Wei, Ying Fu, Yiwei Chu, Luman Wang
{"title":"M2巨噬细胞促进IL-10+ b细胞生成,减轻小鼠哮喘。","authors":"Baichao Yu, Xueqi Wang, Yongkun Zheng, Wenjun Wang, Xiaoqin Cheng, Yue Cao, Mingxing Wei, Ying Fu, Yiwei Chu, Luman Wang","doi":"10.1093/immadv/ltaf007","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>B cells have a central regulatory role in various diseases. While macrophages are found in the disease microenvironment and interact with tissue and diverse immune cells, their relationship with B cells remains poorly explored.</p><p><strong>Methods: </strong>This study used an asthma animal model and macrophage depletion and demonstrated a significant exacerbation of asthma symptoms upon macrophage removal, coupled with a marked reduction in IL-10<sup>+</sup> B-cell expression.</p><p><strong>Results: </strong>Further analysis revealed that the macrophages interacting with IL-10<sup>+</sup> B cells in the asthma microenvironment were of the M2 subtype. Furthermore, our sequencing data indicated a potential mechanism wherein M2 macrophages promote IL-10<sup>+</sup> B-cell activity through the TGF-β pathway and oxidative phosphorylation pathways.</p><p><strong>Conclusion: </strong>These findings suggest that M2 macrophages modulate IL-10<sup>+</sup> B cells, ultimately mitigating asthma symptoms in mouse models.</p>","PeriodicalId":73353,"journal":{"name":"Immunotherapy advances","volume":"5 1","pages":"ltaf007"},"PeriodicalIF":4.1000,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12059559/pdf/","citationCount":"0","resultStr":"{\"title\":\"M2 macrophages promote IL-10<sup>+</sup>B-cell production and alleviate asthma in mice.\",\"authors\":\"Baichao Yu, Xueqi Wang, Yongkun Zheng, Wenjun Wang, Xiaoqin Cheng, Yue Cao, Mingxing Wei, Ying Fu, Yiwei Chu, Luman Wang\",\"doi\":\"10.1093/immadv/ltaf007\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>B cells have a central regulatory role in various diseases. While macrophages are found in the disease microenvironment and interact with tissue and diverse immune cells, their relationship with B cells remains poorly explored.</p><p><strong>Methods: </strong>This study used an asthma animal model and macrophage depletion and demonstrated a significant exacerbation of asthma symptoms upon macrophage removal, coupled with a marked reduction in IL-10<sup>+</sup> B-cell expression.</p><p><strong>Results: </strong>Further analysis revealed that the macrophages interacting with IL-10<sup>+</sup> B cells in the asthma microenvironment were of the M2 subtype. Furthermore, our sequencing data indicated a potential mechanism wherein M2 macrophages promote IL-10<sup>+</sup> B-cell activity through the TGF-β pathway and oxidative phosphorylation pathways.</p><p><strong>Conclusion: </strong>These findings suggest that M2 macrophages modulate IL-10<sup>+</sup> B cells, ultimately mitigating asthma symptoms in mouse models.</p>\",\"PeriodicalId\":73353,\"journal\":{\"name\":\"Immunotherapy advances\",\"volume\":\"5 1\",\"pages\":\"ltaf007\"},\"PeriodicalIF\":4.1000,\"publicationDate\":\"2025-03-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12059559/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Immunotherapy advances\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1093/immadv/ltaf007\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q2\",\"JCRName\":\"IMMUNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Immunotherapy advances","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/immadv/ltaf007","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

B细胞在多种疾病中起着重要的调节作用。虽然巨噬细胞存在于疾病微环境中,并与组织和多种免疫细胞相互作用,但它们与B细胞的关系尚不清楚。方法:本研究采用哮喘动物模型和巨噬细胞去除,发现巨噬细胞去除后哮喘症状显著加重,同时IL-10+ b细胞表达显著降低。结果:进一步分析发现哮喘微环境中与IL-10+ B细胞相互作用的巨噬细胞为M2亚型。此外,我们的测序数据表明,M2巨噬细胞通过TGF-β途径和氧化磷酸化途径促进IL-10+ b细胞活性的潜在机制。结论:这些发现提示M2巨噬细胞调节IL-10+ B细胞,最终减轻小鼠哮喘症状。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
M2 macrophages promote IL-10+B-cell production and alleviate asthma in mice.

Introduction: B cells have a central regulatory role in various diseases. While macrophages are found in the disease microenvironment and interact with tissue and diverse immune cells, their relationship with B cells remains poorly explored.

Methods: This study used an asthma animal model and macrophage depletion and demonstrated a significant exacerbation of asthma symptoms upon macrophage removal, coupled with a marked reduction in IL-10+ B-cell expression.

Results: Further analysis revealed that the macrophages interacting with IL-10+ B cells in the asthma microenvironment were of the M2 subtype. Furthermore, our sequencing data indicated a potential mechanism wherein M2 macrophages promote IL-10+ B-cell activity through the TGF-β pathway and oxidative phosphorylation pathways.

Conclusion: These findings suggest that M2 macrophages modulate IL-10+ B cells, ultimately mitigating asthma symptoms in mouse models.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
CiteScore
5.00
自引率
0.00%
发文量
0
审稿时长
7 weeks
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信