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J Med Virol. 2023 Apr;95(4):e28728. doi: 10.1002/jmv.28728.
3
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Acta Trop. 2023 Jul;243:106931. doi: 10.1016/j.actatropica.2023.106931. Epub 2023 Apr 20.
4
CXCR6+CD4+ T cells promote mortality during Trypanosoma brucei infection.CXCR6+CD4+ T 细胞促进感染布氏锥虫时的死亡率。
PLoS Pathog. 2021 Oct 6;17(10):e1009968. doi: 10.1371/journal.ppat.1009968. eCollection 2021 Oct.
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Helicobacter pylori promote inflammation and host defense through the cagA-dependent activation of mTORC1.幽门螺杆菌通过 cagA 依赖性激活 mTORC1 促进炎症和宿主防御。
J Cell Physiol. 2020 Dec;235(12):10094-10108. doi: 10.1002/jcp.29826. Epub 2020 Jul 28.
6
Translational profiling of macrophages infected with Leishmania donovani identifies mTOR- and eIF4A-sensitive immune-related transcripts.感染杜氏利什曼原虫的巨噬细胞的翻译组谱分析鉴定出 mTOR 和 eIF4A 敏感的免疫相关转录本。
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感染诱导巨噬细胞中趋化因子 CXCL16 的表达,以促进 CXCR6 细胞的趋化吸引。

infection induces the expression of the chemokine CXCL16 in macrophages to promote chemoattraction of CXCR6 cells.

机构信息

Institut National de la Recherche Scientifique (INRS)-Centre Armand-Frappier Santé Biotechnologie (CAFSB), Laval, Québec, Canada.

Department of Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia, Canada.

出版信息

Infect Immun. 2024 Nov 12;92(11):e0030924. doi: 10.1128/iai.00309-24. Epub 2024 Oct 22.

DOI:10.1128/iai.00309-24
PMID:39436058
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11556035/
Abstract

CXCL16 is a multifaceted chemokine expressed by macrophages and other immune cells in response to viral and bacterial pathogens. However, few studies have investigated its role in parasitic infections. The obligate intracellular parasite () is the causative agent of toxoplasmosis, an infection with potentially deleterious consequences in immunocompromised individuals and the developing fetus of acutely infected pregnant women. Chemokines are critical mediators of host defense and, as such, dysregulation of their expression is a subversion strategy often employed by the parasite to ensure its survival. Herein, we report that types I and II strains upregulated the expression of both transmembrane and soluble forms of CXCL16 in infected bone marrow-derived macrophages (BMDM). Exposure to soluble antigens (STAg) and to excreted-secreted proteins (TgESP) led to the induction of CXCL16. mRNA abundance and CXCL16 protein levels increased in a time-dependent manner upon infection. Importantly, conditioned medium (CM) collected from -infected wild-type (WT) macrophage cultures promoted the migration of RAW264.7 cells expressing CXCR6, the cognate receptor of CXCL16, an effect that was significantly reduced by a neutralizing anti-CXCL16 antibody or use of CM from CXCL16 knockout (KO) macrophages. Lastly, -driven CXCL16 expression appeared to modulate cytokine-induced (IL-4 + IL-13) alternative macrophage activation and M2 phenotypic marker expression. Further investigation is required to determine whether this chemokine contributes to the pathogenesis of toxoplasmosis and to elucidate the underlying molecular mechanisms.

摘要

趋化因子 CXCL16 是一种多功能趋化因子,可被巨噬细胞和其他免疫细胞在响应病毒和细菌病原体时表达。然而,很少有研究调查其在寄生虫感染中的作用。专性细胞内寄生虫 ()是弓形虫病的病原体,对于免疫功能低下的个体和急性感染孕妇的胎儿,这种感染具有潜在的有害后果。趋化因子是宿主防御的关键介质,因此,其表达的失调是寄生虫经常采用的颠覆策略,以确保其生存。在此,我们报告 I 型和 II 型 株在感染的骨髓来源巨噬细胞(BMDM)中上调了跨膜和可溶性形式的 CXCL16 的表达。暴露于可溶性 抗原(STAg)和分泌的蛋白质(TgESP)导致 CXCL16 的诱导。在 感染后,CXCL16 的 mRNA 丰度和蛋白水平呈时间依赖性增加。重要的是,从 -感染的野生型(WT)巨噬细胞培养物收集的条件培养基(CM)促进了表达 CXCR6 的 RAW264.7 细胞的迁移,CXCL16 的中和抗体或来自 CXCL16 敲除(KO)巨噬细胞的 CM 显著降低了这种迁移作用。最后,-驱动的 CXCL16 表达似乎调节了细胞因子诱导的(IL-4 + IL-13)替代型巨噬细胞激活和 M2 表型标志物的表达。需要进一步研究以确定这种趋化因子是否有助于弓形虫病的发病机制,并阐明潜在的分子机制。