Complement receptor 3-dependent engagement by Candida glabrata β-glucan modulates dendritic cells to induce regulatory T-cell expansion.

IF 4.5 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Open Biology Pub Date : 2024-05-01 Epub Date: 2024-05-29 DOI:10.1098/rsob.230315
Areerat Kunanopparat, Truc Thi Huong Dinh, Pranpariya Ponpakdee, Panuwat Padungros, Warerat Kaewduangduen, Kasirapat Ariya-Anandech, Phawida Tummamunkong, Amanee Samaeng, Pannagorn Sae-Ear, Asada Leelahavanichkul, Nattiya Hirankarn, Patcharee Ritprajak
{"title":"Complement receptor 3-dependent engagement by <i>Candida glabrata</i> β-glucan modulates dendritic cells to induce regulatory T-cell expansion.","authors":"Areerat Kunanopparat, Truc Thi Huong Dinh, Pranpariya Ponpakdee, Panuwat Padungros, Warerat Kaewduangduen, Kasirapat Ariya-Anandech, Phawida Tummamunkong, Amanee Samaeng, Pannagorn Sae-Ear, Asada Leelahavanichkul, Nattiya Hirankarn, Patcharee Ritprajak","doi":"10.1098/rsob.230315","DOIUrl":null,"url":null,"abstract":"<p><p><i>Candida glabrata</i> is an important pathogen causing invasive infection associated with a high mortality rate. One mechanism that causes the failure of <i>Candida</i> eradication is an increase in regulatory T cells (Treg), which play a major role in immune suppression and promoting <i>Candida</i> pathogenicity. To date, how <i>C. glabrata</i> induces a Treg response remains unclear. Dendritic cells (DCs) recognition of fungi provides the fundamental signal determining the fate of the T-cell response. This study investigated the interplay between <i>C. glabrata</i> and DCs and its effect on Treg induction. We found that <i>C. glabrata</i> β-glucan was a major component that interacted with DCs and consequently mediated the Treg response. Blocking the binding of <i>C. glabrata</i> β-glucan to dectin-1 and complement receptor 3 (CR3) showed that CR3 activation in DCs was crucial for the induction of Treg. Furthermore, a ligand-receptor binding assay showed the preferential binding of <i>C. glabrata</i> β-glucan to CR3. Our data suggest that <i>C. glabrata</i> β-glucan potentially mediates the Treg response, probably through CR3-dependent activation in DCs. This study contributes new insights into immune modulation by <i>C. glabrata</i> that may lead to a better design of novel immunotherapeutic strategies for invasive <i>C. glabrata</i> infection.</p>","PeriodicalId":19629,"journal":{"name":"Open Biology","volume":"14 5","pages":"230315"},"PeriodicalIF":4.5000,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11293457/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Open Biology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1098/rsob.230315","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/5/29 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Candida glabrata is an important pathogen causing invasive infection associated with a high mortality rate. One mechanism that causes the failure of Candida eradication is an increase in regulatory T cells (Treg), which play a major role in immune suppression and promoting Candida pathogenicity. To date, how C. glabrata induces a Treg response remains unclear. Dendritic cells (DCs) recognition of fungi provides the fundamental signal determining the fate of the T-cell response. This study investigated the interplay between C. glabrata and DCs and its effect on Treg induction. We found that C. glabrata β-glucan was a major component that interacted with DCs and consequently mediated the Treg response. Blocking the binding of C. glabrata β-glucan to dectin-1 and complement receptor 3 (CR3) showed that CR3 activation in DCs was crucial for the induction of Treg. Furthermore, a ligand-receptor binding assay showed the preferential binding of C. glabrata β-glucan to CR3. Our data suggest that C. glabrata β-glucan potentially mediates the Treg response, probably through CR3-dependent activation in DCs. This study contributes new insights into immune modulation by C. glabrata that may lead to a better design of novel immunotherapeutic strategies for invasive C. glabrata infection.

依赖补体受体 3 的胶状念珠菌β-葡聚糖可调节树突状细胞,从而诱导调节性 T 细胞扩增。
白色念珠菌是一种重要的病原体,可导致与高死亡率相关的侵袭性感染。导致念珠菌根除失败的一个机制是调节性 T 细胞(Treg)的增加,Treg 在免疫抑制和促进念珠菌致病性方面发挥着重要作用。迄今为止,人们仍不清楚光滑念珠菌是如何诱导 Treg 反应的。树突状细胞(DC)对真菌的识别提供了决定 T 细胞反应命运的基本信号。本研究调查了青霉与 DCs 之间的相互作用及其对 Treg 诱导的影响。我们发现,草履蛆β-葡聚糖是与DC相互作用的主要成分,并因此介导了Treg反应。阻断草履虫β-葡聚糖与脱落素-1和补体受体3(CR3)的结合表明,直流细胞中CR3的活化是诱导Treg的关键。此外,配体-受体结合试验显示,C. glabrata β-葡聚糖优先与 CR3 结合。我们的数据表明,草履虫β-葡聚糖可能通过依赖于CR3的DCs活化介导Treg反应。这项研究有助于我们深入了解草履蛆对免疫的调节作用,从而更好地设计新型免疫治疗策略来治疗侵袭性草履蛆感染。
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 求助全文
来源期刊
Open Biology
Open Biology BIOCHEMISTRY & MOLECULAR BIOLOGY-
CiteScore
10.00
自引率
1.70%
发文量
136
审稿时长
6-12 weeks
期刊介绍: Open Biology is an online journal that welcomes original, high impact research in cell and developmental biology, molecular and structural biology, biochemistry, neuroscience, immunology, microbiology and genetics.
×
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