Biological relevance of A2a receptor in Schwann cells infected by Mycobacterium leprae: a possible pathway involved in leprosy?

Plínio Marcos Freire dos Santos, B. S. Mietto, L. Gutierres, Antônio Marcos Rodrigues Pereira, C. C. Acosta, M. C. Pessolani, Marcia de Berrêdo Pinho Moreira
{"title":"Biological relevance of A2a receptor in Schwann cells infected by Mycobacterium leprae: a possible pathway involved in leprosy?","authors":"Plínio Marcos Freire dos Santos, B. S. Mietto, L. Gutierres, Antônio Marcos Rodrigues Pereira, C. C. Acosta, M. C. Pessolani, Marcia de Berrêdo Pinho Moreira","doi":"10.35259/ISI.SACT.2019_32833","DOIUrl":null,"url":null,"abstract":"Introduction: Leprosy is a chronic infectious disease caused by Mycobacterium leprae which evokes a strong inflammatory response and leads to nerve damage. Two important aspects that favor the establishment of infection and survival of M. leprae are: lipid droplet accumulation and the capacity to induce rapid demyelination after extracellular binding to myelinating Schwann cells (SC). Recently, purinergic receptors have been shown to participate in myelination processes, lipid metabolism and immune response. In addition, the purinergic signaling system plays an important role by modulating inflammatory and immune responses, via extracellular adenine nucleotides and their derived nucleoside adenosine (ADO). The enzymatic activities of CD39, CD73 and Adenosine deaminase play strategic roles in regulating purinergic signals through the conversion of ADP/ATP to AMP, AMP to adenosine and adenosine to inosine respectively.","PeriodicalId":427855,"journal":{"name":"Anais do IV International Symposium on Immunobiological e VII Seminário Anual Científico e Tecnológico de Bio-Manguinhos","volume":"141 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Anais do IV International Symposium on Immunobiological e VII Seminário Anual Científico e Tecnológico de Bio-Manguinhos","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.35259/ISI.SACT.2019_32833","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Introduction: Leprosy is a chronic infectious disease caused by Mycobacterium leprae which evokes a strong inflammatory response and leads to nerve damage. Two important aspects that favor the establishment of infection and survival of M. leprae are: lipid droplet accumulation and the capacity to induce rapid demyelination after extracellular binding to myelinating Schwann cells (SC). Recently, purinergic receptors have been shown to participate in myelination processes, lipid metabolism and immune response. In addition, the purinergic signaling system plays an important role by modulating inflammatory and immune responses, via extracellular adenine nucleotides and their derived nucleoside adenosine (ADO). The enzymatic activities of CD39, CD73 and Adenosine deaminase play strategic roles in regulating purinergic signals through the conversion of ADP/ATP to AMP, AMP to adenosine and adenosine to inosine respectively.
麻风分枝杆菌感染雪旺细胞中A2a受体的生物学相关性:参与麻风的可能途径?
简介:麻风是一种由麻风分枝杆菌引起的慢性传染病,可引起强烈的炎症反应并导致神经损伤。有利于麻风分枝杆菌感染和存活的两个重要方面是:脂滴积累和细胞外结合成髓鞘的雪旺细胞(SC)后诱导快速脱髓鞘的能力。近年来,嘌呤能受体已被证明参与髓鞘形成过程、脂质代谢和免疫反应。此外,嘌呤能信号系统通过胞外腺嘌呤核苷酸及其衍生的核苷腺苷(ADO)在调节炎症和免疫反应中发挥重要作用。CD39、CD73和腺苷脱氨酶的酶活性分别通过ADP/ATP转化为AMP、AMP转化为腺苷和腺苷转化为肌苷,在调节嘌呤能信号中发挥战略性作用。
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 求助全文
来源期刊
自引率
0.00%
发文量
0
×
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:604180095
Book学术官方微信