Entamoeba histolytica Develops Resistance to Complement Deposition and Lysis after Acquisition of Human Complement-Regulatory Proteins through Trogocytosis.
Entamoeba histolytica Develops Resistance to Complement Deposition and Lysis after Acquisition of Human Complement-Regulatory Proteins through Trogocytosis.
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DOI：
10.1128/mbio.03163-21
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发表时间：
2022-04-26
期刊：
影响因子：
6.4
通讯作者：
Ralston KS
中科院分区：
文献类型：
--
作者：
Miller HW;Tam TSY;Ralston KS
溶组织内阿米巴是阿米巴病的病因。这种寄生虫的滋养体（变形虫）形式能够侵入肠道，并可以通过血液传播到其他器官。阿米巴原虫在传播过程中逃避补体沉积的机制尚未得到很好的表征。我们以前发现了一种新的补体逃避机制所采用的E。溶组织剂E.溶组织菌在称为胞啃的过程中摄取少量的活的人类细胞。我们证明，阿米巴受人血清胞吞作用后的人细胞和阿米巴收购和展示人类膜蛋白从他们摄入的细胞裂解。在这里，我们的目的是确定阿米巴是如何保护补体裂解后进行胞刺。我们发现，阿米巴受保护，从补体裂解后摄入的人Jurkat T细胞和红细胞，保护水平与摄入的材料量相关。人类细胞的胞吞作用导致阿米巴原虫表面C3b沉积减少。我们询问人类补体调节因子的展示是否参与阿米巴保护，发现CD59在胞啃后被阿米巴展示。从Jurkat细胞中删除单个补体调节蛋白CD59或CD46不足以改变阿米巴对溶解的保护，这表明多个冗余的补体调节剂介导阿米巴保护。然而，外源性表达的CD46或CD55阿米巴是足以提供保护，从溶解。这些研究揭示了病原体免疫逃避的新策略。
Entamoeba histolytica is the cause of amoebiasis. The trophozoite (amoeba) form of this parasite is capable of invading the intestine and can disseminate through the bloodstream to other organs. The mechanisms that allow amoebae to evade complement deposition during dissemination have not been well characterized. We previously discovered a novel complement-evasion mechanism employed by E. histolytica. E. histolytica ingests small bites of living human cells in a process termed trogocytosis. We demonstrated that amoebae were protected from lysis by human serum following trogocytosis of human cells and that amoebae acquired and displayed human membrane proteins from the cells they ingested. Here, we aimed to define how amoebae are protected from complement lysis after performing trogocytosis. We found that amoebae were protected from complement lysis after ingestion of both human Jurkat T cells and red blood cells and that the level of protection correlated with the amount of material ingested. Trogocytosis of human cells led to a reduction in deposition of C3b on the surface of amoebae. We asked whether display of human complement regulators is involved in amoebic protection, and found that CD59 was displayed by amoebae after trogocytosis. Deletion of a single complement-regulatory protein, CD59 or CD46, from Jurkat cells was not sufficient to alter amoebic protection from lysis, suggesting that multiple, redundant complement regulators mediate amoebic protection. However, exogeneous expression of CD46 or CD55 in amoebae was sufficient to confer protection from lysis. These studies shed light on a novel strategy for immune evasion by a pathogen.
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影响因子：
64.8
作者：
通讯作者：
--
DOI：
10.14740/jocmr2131w
发表时间：
2015-06-01
期刊：
Journal of clinical medicine research
影响因子：
--
作者：
Alvarado-Esquivel, Cosme;Hernandez-Tinoco, Jesus;Sanchez-Anguiano, Luis Francisco
通讯作者：
Sanchez-Anguiano, Luis Francisco
影响因子：
6.4
作者：
Miller, Hannah W.;Suleiman, Rene L.;Ralston, Katherine S.
通讯作者：
Ralston, Katherine S.
影响因子：
3.4
作者：
GONZALEZRUIZ, A;HAQUE, R;WARHURST, DC
通讯作者：
WARHURST, DC
影响因子：
3.2
作者：
Costa, Cassia A. X.;Nunes, Alvaro C.;Caliari, Marcelo V.
通讯作者：
Caliari, Marcelo V.