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促进还是抑制:疟疾中的免疫调节剂。

Accelerator or Brake: Immune Regulators in Malaria.

机构信息

Research Center for High Altitude Medicine, School of Medical, Qinghai University, Xining, China.

Key Laboratory of Application and Foundation for High Altitude Medicine Research in Qinghai Province, Qinghai University, Xining, China.

出版信息

Front Cell Infect Microbiol. 2020 Dec 10;10:610121. doi: 10.3389/fcimb.2020.610121. eCollection 2020.

DOI:10.3389/fcimb.2020.610121
PMID:33363057
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7758250/
Abstract

Malaria is a life-threatening infectious disease, affecting over 250 million individuals worldwide each year, eradicating malaria has been one of the greatest challenges to public health for a century. Growing resistance to anti-parasitic therapies and lack of effective vaccines are major contributing factors in controlling this disease. However, the incomplete understanding of parasite interactions with host anti-malaria immunity hinders vaccine development efforts to date. Recent studies have been unveiling the complexity of immune responses and regulators against infection. Here, we summarize our current understanding of host immune responses against -derived components infection and mainly focus on the various regulatory mechanisms mediated by recent identified immune regulators orchestrating anti-malaria immunity.

摘要

疟疾是一种危及生命的传染病,每年在全球影响超过 2.5 亿人,消除疟疾是一个多世纪以来公共卫生面临的最大挑战之一。寄生虫对抗寄生虫疗法的耐药性增加和缺乏有效的疫苗是控制这种疾病的主要因素。然而,对寄生虫与宿主抗疟免疫相互作用的不完全了解阻碍了迄今为止的疫苗开发工作。最近的研究揭示了针对感染的免疫反应和调节剂的复杂性。在这里,我们总结了我们对宿主针对疟原虫衍生成分感染的免疫反应的现有理解,主要集中在最近发现的调节免疫的各种调节机制上,这些机制协调了抗疟免疫。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/497f/7758250/0cc0fc589f1e/fcimb-10-610121-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/497f/7758250/2f3d0bfd7ea7/fcimb-10-610121-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/497f/7758250/0cc0fc589f1e/fcimb-10-610121-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/497f/7758250/2f3d0bfd7ea7/fcimb-10-610121-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/497f/7758250/0cc0fc589f1e/fcimb-10-610121-g002.jpg

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