Cytokines and splenic remodelling during Leishmania donovani infection

Q1 Medicine Cytokine: X Pub Date : 2020-12-01 DOI:10.1016/j.cytox.2020.100036
Marcela Montes de Oca , Christian R. Engwerda , Paul M. Kaye
{"title":"Cytokines and splenic remodelling during Leishmania donovani infection","authors":"Marcela Montes de Oca ,&nbsp;Christian R. Engwerda ,&nbsp;Paul M. Kaye","doi":"10.1016/j.cytox.2020.100036","DOIUrl":null,"url":null,"abstract":"<div><p>Visceral leishmaniasis (VL) causes extensive splenic pathology that contributes to dysfunctional immune responses, in part through displacement and destruction of cell populations involved in maintaining splenic structural integrity. The expression of pro and anti-inflammatory cytokines and chemokines is crucial in orchestrating the delicate balance that exists between host resistance and tissue pathology. In an effort to restore homeostatic balance to the local microenvironment, remodelling of the splenic architecture occurs in a compartmentalised manner to retain some level of functionality, despite persistent inflammatory pressures. Animal models of VL as well as human studies have significantly contributed to our understanding of the architectural changes that occur in the spleen during VL. Here, we review the role of cytokines in mediating microarchitectural changes associated with the development of splenomegaly during VL.</p></div>","PeriodicalId":37028,"journal":{"name":"Cytokine: X","volume":"2 4","pages":"Article 100036"},"PeriodicalIF":0.0000,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cytox.2020.100036","citationCount":"8","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cytokine: X","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2590153220300161","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 8

Abstract

Visceral leishmaniasis (VL) causes extensive splenic pathology that contributes to dysfunctional immune responses, in part through displacement and destruction of cell populations involved in maintaining splenic structural integrity. The expression of pro and anti-inflammatory cytokines and chemokines is crucial in orchestrating the delicate balance that exists between host resistance and tissue pathology. In an effort to restore homeostatic balance to the local microenvironment, remodelling of the splenic architecture occurs in a compartmentalised manner to retain some level of functionality, despite persistent inflammatory pressures. Animal models of VL as well as human studies have significantly contributed to our understanding of the architectural changes that occur in the spleen during VL. Here, we review the role of cytokines in mediating microarchitectural changes associated with the development of splenomegaly during VL.

Abstract Image

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
多诺瓦利什曼原虫感染期间细胞因子和脾重构
内脏利什曼病(VL)引起广泛的脾病理,导致免疫反应功能失调,部分原因是参与维持脾结构完整性的细胞群移位和破坏。促炎性和抗炎性细胞因子和趋化因子的表达在协调宿主抵抗和组织病理之间的微妙平衡中至关重要。为了恢复局部微环境的稳态平衡,脾结构的重塑以分区的方式发生,以保持一定程度的功能,尽管持续的炎症压力。VL的动物模型和人体研究对我们理解VL期间脾脏的结构变化有重要贡献。在这里,我们回顾细胞因子在介导与VL期间脾肿大发展相关的微结构变化中的作用。
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
Cytokine: X
Cytokine: X Medicine-Hematology
CiteScore
13.20
自引率
0.00%
发文量
6
审稿时长
15 weeks
期刊最新文献
Editorial Board Progress of exosome research in systemic lupus erythematosus Editorial Board TNFAIP8 modulates the survival and immune activity of Th17 cells via p53/ p21/ MDM2 pathway after acute insult An exploratory study of circulating cytokines and chemokines in patients with muscle disorders proposes CD40L and CCL5 represent general disease markers while CXCL10 differentiates between patients with an autoimmune myositis
×
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