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来自[具体来源未提及]的重组微线体蛋白MIC1和MIC4对人Jurkat T淋巴细胞系具有细胞毒性作用。

Recombinant Microneme Proteins MIC1 and MIC4 from Cause Cytotoxic Effects in the Human Jurkat T-Lymphocyte Cell Line.

作者信息

Souza Igor E L, Roque-Barreira Maria-Cristina, Panunto-Castelo Ademilson

机构信息

Department of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto 14040-901, SP, Brazil.

Department of Biology, Faculty of Philosophy, Sciences and Letters at Ribeirão Preto, Ribeirão Preto 14040-901, SP, Brazil.

出版信息

Pathogens. 2025 Apr 9;14(4):372. doi: 10.3390/pathogens14040372.

DOI:10.3390/pathogens14040372
PMID:40333130
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12030039/
Abstract

is an obligate intracellular parasite that causes toxoplasmosis, a potentially devastating disease to fetuses and immunocompromised individuals. Among its microneme proteins, MIC1 and MIC4 play crucial roles in host-parasite interactions, facilitating adhesion by binding glycans on host cells. Beyond these roles, these lectins have been implicated in modulating immune responses and inducing apoptosis, but their effects on human immune cells remain unclear. Here, we investigated the interaction of recombinant MIC1 (rMIC1) and rMIC4 with Jurkat T lymphocytes, a human immune cell model. Both lectins bound Jurkat cells in a carbohydrate-dependent manner, with rMIC4 showing competitive binding over rMIC1. Importantly, we observed that rMIC1 and rMIC4 reduced Jurkat cell viability in a time- and dose-dependent manner, inducing apoptosis through caspase activation by extrinsic and intrinsic pathways. The apoptosis was driven by reactive oxygen species production via the NADPH oxidase complex and the activation of p38 and JNK MAPK signaling pathways, emphasizing the ability of these lectins to modulate cellular signaling cascades. This study offers insights into the mechanisms involved in MIC1 and MIC4 interactions with immune cells.

摘要

是一种专性细胞内寄生虫，可导致弓形虫病，这是一种对胎儿和免疫功能低下个体可能具有毁灭性的疾病。在其微线体蛋白中，MIC1和MIC4在宿主-寄生虫相互作用中起关键作用，通过结合宿主细胞上的聚糖促进黏附。除了这些作用外，这些凝集素还与调节免疫反应和诱导细胞凋亡有关，但其对人类免疫细胞的影响仍不清楚。在这里，我们研究了重组MIC1（rMIC1）和rMIC4与人类免疫细胞模型Jurkat T淋巴细胞的相互作用。两种凝集素均以碳水化合物依赖性方式结合Jurkat细胞，rMIC4对rMIC1表现出竞争性结合。重要的是，我们观察到rMIC1和rMIC4以时间和剂量依赖性方式降低Jurkat细胞活力，通过外在和内在途径激活半胱天冬酶诱导细胞凋亡。细胞凋亡由通过NADPH氧化酶复合物产生的活性氧以及p38和JNK MAPK信号通路的激活驱动，强调了这些凝集素调节细胞信号级联反应的能力。这项研究为MIC1和MIC4与免疫细胞相互作用的机制提供了见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29ba/12030039/69b8db80574a/pathogens-14-00372-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29ba/12030039/ab9bfae96d45/pathogens-14-00372-g005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29ba/12030039/914e3756b7c9/pathogens-14-00372-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29ba/12030039/69b8db80574a/pathogens-14-00372-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29ba/12030039/0fb1dd852ec4/pathogens-14-00372-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29ba/12030039/4e6f601c3a22/pathogens-14-00372-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29ba/12030039/85d85552747d/pathogens-14-00372-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29ba/12030039/de7d497c1cfe/pathogens-14-00372-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29ba/12030039/ab9bfae96d45/pathogens-14-00372-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29ba/12030039/ce40bc9b0524/pathogens-14-00372-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29ba/12030039/914e3756b7c9/pathogens-14-00372-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29ba/12030039/69b8db80574a/pathogens-14-00372-g008.jpg

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本文引用的文献

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Pathogens. 2024 Nov 6;13(11):968. doi: 10.3390/pathogens13110968.
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The role of IFN-γ-mediated host immune responses in monitoring and the elimination of Toxoplasma gondii infection.IFN-γ 介导的宿主免疫反应在监测和消除弓形虫感染中的作用。
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The fungal Clitocybe nebularis lectin binds distinct cell surface glycoprotein receptors to induce cell death selectively in Jurkat cells.真菌云芝凝集素通过结合不同的细胞表面糖蛋白受体，选择性诱导 Jurkat 细胞死亡。
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Microneme Proteins 1 and 4 From Induce IL-10 Production by Macrophages Through TLR4 Endocytosis.微刺蛋白 1 和 4 通过 TLR4 内吞作用诱导巨噬细胞产生 IL-10。
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