Enterocyte–ILC1 crosstalk drives innate IFN-g-mediated control of Cryptosporidium

Cryptosporidium infects enterocytes, but their contribution to parasite control is not well understood. Early resistance to Cryptosporidium is dependent on the production of IFN gamma. Loss of STAT1 in enterocytes, but not dendritic cells or macrophages, antagonized early parasite control. Moreover, transcriptional profiling of enterocytes from infected mice revealed the induction of an IFN gamma signature that included multiple genes (IDO, GBP, IRG) associated with control of intracellular pathogens. Overall design: Two-three biological replicates were analyzed for each of 3 conditions (uninfected vs infected for 3 or 5 days)

隐孢子虫（Cryptosporidium）可侵染肠上皮细胞（enterocytes），但肠上皮细胞在寄生虫防控中的具体作用尚未被充分阐明。宿主针对隐孢子虫的早期免疫抗性依赖于干扰素γ（IFN-γ）的产生。肠上皮细胞中信号转导与转录激活因子1（STAT1）的缺失，而非树突状细胞或巨噬细胞的STAT1缺失，会拮抗宿主对寄生虫的早期防控能力。此外，对感染小鼠的肠上皮细胞进行转录谱分析后发现，其诱导产生了干扰素γ特征基因表达谱，其中包含多个与胞内病原体防控相关的基因：吲哚胺2,3-双加氧酶（IDO）、鸟苷酸结合蛋白（GBP）以及免疫相关GTP酶（IRG）。实验整体设计：针对3组实验条件（未感染对照组、感染3天组与感染5天组），每组均设置2至3个生物学重复样本进行分析。