NOD1 Agonist Induces Proliferation and Plasma Cell Differentiation of Mouse B Cells Especially CD23high B Cells.

IF 2.9 4区 医学 Q3 IMMUNOLOGY Immunological Investigations Pub Date : 2024-11-19 DOI:10.1080/08820139.2024.2428788
Cendrine Seguin, Michelle Seif, Célia Jacoberger-Foissac, Philippe Gentine, May Wantz, Benoit Frisch, Béatrice Heurtault, Sylvie Fournel
{"title":"NOD1 Agonist Induces Proliferation and Plasma Cell Differentiation of Mouse B Cells Especially CD23<sup>high</sup> B Cells.","authors":"Cendrine Seguin, Michelle Seif, Célia Jacoberger-Foissac, Philippe Gentine, May Wantz, Benoit Frisch, Béatrice Heurtault, Sylvie Fournel","doi":"10.1080/08820139.2024.2428788","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Like innate cells, B cells also express Pattern Recognition Receptors (PRRs) to detect danger signal such as tissue damage or pathogen intrusion. Production of specific antibodies by plasma cells results from the activation and differentiation of B cells following three signals: (i) antigen recognition by B Cell Receptors, (ii) recognition of danger and (iii) T-cell help. However, it is unclear whether T-cell help is dispensable for B cell activation and differentiation or not. Few studies have investigated the role of cytosolic PRRs such as NOD1 in B cell differentiation.</p><p><strong>Methods: </strong>We used splenic C57BL6J B cells to evaluate NOD1 expression and then assessed the effect of stimulation with C12-iE-DAP, a NOD1 ligand, with or without CD40L as a T-cell help signal on B-cell responses globally or according to their CD23 expression level.</p><p><strong>Results: </strong>We showed that murine B cells express NOD1 and that the presence of C12-iE-DAP induces activation, proliferation and initiates differentiation in plasma cells even in the absence of a T-dependent signal. Surprisingly, CD23<sup>high</sup> B cells are more sensitive than CD23<sup>low</sup> B cells to stimulation.</p><p><strong>Conclusion: </strong>Our results suggest that the NLR pathway could induce antibody development during infections and be exploited to develop more effective vaccination.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-15"},"PeriodicalIF":2.9000,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Immunological Investigations","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/08820139.2024.2428788","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Like innate cells, B cells also express Pattern Recognition Receptors (PRRs) to detect danger signal such as tissue damage or pathogen intrusion. Production of specific antibodies by plasma cells results from the activation and differentiation of B cells following three signals: (i) antigen recognition by B Cell Receptors, (ii) recognition of danger and (iii) T-cell help. However, it is unclear whether T-cell help is dispensable for B cell activation and differentiation or not. Few studies have investigated the role of cytosolic PRRs such as NOD1 in B cell differentiation.

Methods: We used splenic C57BL6J B cells to evaluate NOD1 expression and then assessed the effect of stimulation with C12-iE-DAP, a NOD1 ligand, with or without CD40L as a T-cell help signal on B-cell responses globally or according to their CD23 expression level.

Results: We showed that murine B cells express NOD1 and that the presence of C12-iE-DAP induces activation, proliferation and initiates differentiation in plasma cells even in the absence of a T-dependent signal. Surprisingly, CD23high B cells are more sensitive than CD23low B cells to stimulation.

Conclusion: Our results suggest that the NLR pathway could induce antibody development during infections and be exploited to develop more effective vaccination.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
NOD1 激动剂诱导小鼠 B 细胞尤其是 CD23 高 B 细胞增殖和浆细胞分化
背景:与先天性细胞一样,B细胞也表达模式识别受体(PRR),以检测组织损伤或病原体入侵等危险信号。浆细胞产生特异性抗体源于 B 细胞在三种信号下的活化和分化:(i) B 细胞受体识别抗原;(ii) 识别危险;(iii) T 细胞帮助。然而,T 细胞的帮助对于 B 细胞的活化和分化是否不可或缺尚不清楚。很少有研究调查细胞膜 PRRs(如 NOD1)在 B 细胞分化中的作用:方法:我们使用脾脏 C57BL6J B 细胞来评估 NOD1 的表达,然后根据 B 细胞的 CD23 表达水平,评估在使用或不使用 CD40L 作为 T 细胞帮助信号的情况下,NOD1 配体 C12-iE-DAP 刺激对 B 细胞整体反应的影响:结果:我们发现小鼠 B 细胞表达 NOD1,即使没有 T 依赖性信号,C12-iE-DAP 的存在也能诱导浆细胞活化、增殖和分化。令人惊讶的是,CD23高的B细胞比CD23低的B细胞对刺激更敏感:我们的研究结果表明,NLR 途径可在感染过程中诱导抗体的产生,并可用于开发更有效的疫苗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Immunological Investigations
Immunological Investigations 医学-免疫学
CiteScore
5.50
自引率
7.10%
发文量
49
审稿时长
3 months
期刊介绍: Disseminating immunological developments on a worldwide basis, Immunological Investigations encompasses all facets of fundamental and applied immunology, including immunohematology and the study of allergies. This journal provides information presented in the form of original research articles and book reviews, giving a truly in-depth examination of the latest advances in molecular and cellular immunology.
期刊最新文献
Differential Expression of Granulysin, MHC Class I-Related Chain A, and Perforin in Serum and Peritoneal Fluid: Immune Dysregulation in Endometriosis-Related Infertility. Serum-Derived Exosomal TBX2-AS1 Exacerbates COPD by Altering the M1/M2 Ratio of Macrophages through Regulating the miR-423-5p/miR-23b-3p Axis. Evaluation of the Immunoadjuvant Effects of miR-155-Chitosan Polyplex on Leishmania major Infected Mice. Combination Effect of Radiotherapy and Targeted Therapy with NK Cell-Based Immunotherapy in head and Neck Squamous Cell Carcinoma. NOD1 Agonist Induces Proliferation and Plasma Cell Differentiation of Mouse B Cells Especially CD23high B Cells.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1