Fam96a is essential for the host control of Toxoplasma gondii infection by fine-tuning macrophage polarization via an iron-dependent mechanism

Fam96a 通过铁依赖机制微调巨噬细胞极化,对宿主控制弓形虫感染至关重要

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作者:Zhuanzhuan Liu, Hanying Wang, Zhiwei Zhang, Yulu Ma, Qiyue Jing, Shenghai Zhang, Jinzhi Han, Junru Chen, Yaoyao Xiang, Yanbo Kou, Yanxia Wei, Lu Wang, Yugang Wang

Background

Toxoplasmosis affects a quarter of the world's population. Toxoplasma gondii (T.gondii) is an intracellular parasitic protozoa. Macrophages are necessary for proliferation and spread of T.gondii by regulating immunity and metabolism. Family with sequence similarity 96A (Fam96a; formally named Ciao2a) is an evolutionarily conserved protein that is highly expressed in macrophages, but whether it play a role in control of T. gondii infection is unknown. Methodology/principal findings: In this study, we utilized myeloid cell-specific knockout mice to test its role in anti-T. gondii immunity. The

Significance

All these findings suggest that Fam96a ablation in macrophages disrupts iron homeostasis and inhibits immune effector molecules, which may aggravate both acute and chronic toxoplasmosis. It highlights that Fam96a may autonomously act as a critical gatekeeper of T. gondii control in macrophages.

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