4.6 Article

C-type lectin 4 regulates broad-spectrum melanization-based refractoriness to malaria parasites

期刊

PLOS BIOLOGY
卷 20, 期 1, 页码 -

出版社

PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pbio.3001515

关键词

-

资金

  1. National Institutes of Health [R21AI131574]
  2. Bloomberg Philanthropies
  3. University of California Irvine Malaria Initiative
  4. Johns Hopkins Malaria Research Institute Postdoctoral Fellowship

向作者/读者索取更多资源

Using CRISPR/Cas9-based gene editing, this study reveals that Anopheles gambiae mosquitos can mount melanization-based refractoriness to the human malaria parasite, independent of traditional immune pathways. The study identifies CTL4 as an essential host factor for P. falciparum transmission.
Anopheles gambiae melanization-based refractoriness to the human malaria parasite Plasmodium falciparum has rarely been observed in either laboratory or natural conditions, in contrast to the rodent model malaria parasite Plasmodium berghei that can become completely melanized by a TEP1 complement-like system-dependent mechanism. Multiple studies have shown that the rodent parasite evades this defense by recruiting the C-type lectins CTL4 and CTLMA2, while permissiveness to the human malaria parasite was not affected by partial depletion of these factors by RNAi silencing. Using CRISPR/Cas9-based CTL4 knockout, we show that A. gambiae can mount melanization-based refractoriness to the human malaria parasite, which is independent of the TEP1 complement-like system and the major anti-Plasmodium immune pathway Imd. Our study indicates a hierarchical specificity in the control of Plasmodium melanization and proves CTL4 as an essential host factor for P. falciparum transmission and one of the most potent mosquito-encoded malaria transmission-blocking targets.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.6
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据