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杆菌利用CD44作为红细胞入侵的核心受体

Barbara Baro¹, Chi Yong Kim¹, Carrie Lin¹

¹Department of Pediatrics, Stanford University School of Medicine, Stanford, CA.

|October 13, 2023

概括

疟疾寄生虫Plasmodium falciparum在红细胞上使用CD44作为入侵的共同受体. 这种相互作用涉及EBA-175和EBA-140连接体,改变红细胞结构以促进寄生虫的进入.

科学领域:

细胞生物学细胞生物学
寄生虫学的寄生虫学
免疫学免疫学免疫学

背景情况:

菌感染人类红细胞,利用宿主因素进行入侵.
CD44以前被确定为疟疾寄生虫感染的潜在宿主因子.
寄生虫入侵期间红细胞中CD44的确切作用和调节尚不清楚.

研究的目的:

在Plasmodium falciparum入侵期间研究CD44在人体红细胞中的功能.
为了识别与CD44.4相互作用的Plasmodium falciparum入侵配体.
阐明CD44促进寄生虫进入的机制.

主要方法:

通过CRISPR/Cas9基因组编辑,在造血干细胞中删除CD44.
活体红细胞生成生成CD44-null和野生类型的培养红细胞 (cRBC).
测试以测量Plasmodium falciparum入侵率,并确定连接体-受体相互作用 (EBA-175,EBA-140与CD44,糖A,糖C).
对红细胞细胞骨蛋白的CD44依赖酸化的分析.

主要成果:

CD44的删除没有影响红质形成,但显著降低了cRBC中的Plasmodium falciparum入侵率.
红细胞结合抗原175 (EBA-175) 和EBA-140被确定为CD44的结合伙伴.
EBA-175与红细胞的结合主要由甘氨酸A介导,而EBA-140与甘氨酸C结合.
EBA-175诱导了红细胞细胞骨蛋白的CD44依赖酸化,改变了细胞的可变性.

结论:

CD44是Plasmodium falciparum侵入人类红细胞的关键共同受体.
寄生虫利用CD44调节宿主细胞的特性,从而促进进入.
这项研究揭示了一种新的疟疾寄生虫入侵机制,涉及CD44和红细胞细胞骨动态.

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