猫在袋子里:刚地弓形虫提供了对髓细胞介导的宿主防御的进一步了解。

Q3 Medicine
Madison L Schanz, Fengdi Zhao, Kamryn E Zadeii, Li Chen, Américo H López-Yglesias
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引用次数: 0

摘要

专性细胞内原生动物病原体弓形虫估计感染了世界上三分之一的人口。弓形虫病被认为是一种重要的世界性疾病,可导致免疫功能低下个体的发病或死亡。宿主对弓形虫的防御已被证明依赖于快速的髓细胞和淋巴细胞反应,协同工作以迅速消除入侵的病原体。传统上,依赖T- β的1组先天淋巴细胞(ILC1s)、自然杀伤细胞(NK)和CD4+ T细胞衍生的干扰素-γ (IFN-γ)被认为是宿主抵抗弓形虫必不可少的。然而,最近的发现表明NK细胞或CD4+ T细胞衍生的IFN-γ不需要T-bet。然而,缺乏T-bet仍然会导致快速死亡,这表明T-bet依赖于骨髓细胞介导的宿主防御途径。本文综述了髓细胞介导的针对弓形虫的免疫反应,并提供了对t- bet依赖的髓细胞依赖宿主防御途径中鲜为人知的病原体清除成分的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The cat's out of the bag: Toxoplasma gondii provides further insight into myeloid-mediated host defense.

The cat's out of the bag: Toxoplasma gondii provides further insight into myeloid-mediated host defense.

The cat's out of the bag: Toxoplasma gondii provides further insight into myeloid-mediated host defense.

The cat's out of the bag: Toxoplasma gondii provides further insight into myeloid-mediated host defense.

The obligate intracellular protozoan pathogen Toxoplasma gondii is estimated to infect a third of the world's population. Toxoplasmosis is considered a significant worldwide disease that can lead to morbidity or death in immunocompromised individuals. Host defense against T. gondii has been demonstrated to be dependent on a rapid myeloid cell and lymphocyte response working in concert to quickly eliminate the invading pathogen. Classically, T-bet-dependent group 1 innate lymphocytes (ILC1s), natural killer (NK) cells, and CD4+ T cell-derived interferon-γ (IFN-γ) are considered indispensable for host resistance against T. gondii. However, recent discoveries have illustrated that T-bet is not required for NK cell- or CD4+ T cell-derived IFN-γ. Yet, lack of T-bet still results in rapid mortality, pointing to a T-bet-dependent myeloid cell-mediated host defense pathway. This review summarizes the myeloid cell-mediated immune response against T. gondii and provides insights into the lesser known components of the T-bet-dependent myeloid cell-dependent host defense pathway for pathogen clearance.

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来源期刊
CiteScore
3.70
自引率
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