目的 探究小鼠多房棘球蚴感染过程中干扰素诱导跨膜蛋白3（IFITM3）与叉头框P3蛋白（Foxp3）相互作用关系。方法 从保种沙鼠肝脏组织中收集多房棘球蚴原头节，腹腔注射建立多房棘球蚴感染C57BL/6J小鼠模型。分别于感染后15、30、60、90 d安乐处死小鼠收集肝脏组织，设置未感染对照组。通过苏木精-伊红（HE）染色法，Masson染色和免疫组化染色观察不同感染时间点小鼠肝脏组织病理变化。通过蛋白质免疫印迹（Western blotting）进一步检测肝组织IFITM3和Foxp3蛋白的相对表达量。HEK-293T细胞转染IFITM3-ShRNA干扰质粒（ShIFITM3-1、ShIFITM3-2、ShIFITM3-3），筛选最优敲低片段进行剂量依赖性实验（以0、0.5、1.0、1.5、2.0 μg转染），进一步检测Foxp3表达变化。采用AutoDock软件进行IFITM3-Foxp3分子对接分析，随后将带标签质粒HA-IFITM3与Flag-Foxp3a转染至HEK-293T细胞中，提取细胞总蛋白，进行免疫共沉淀验证二者相互作用。结果 HE染色结果显示，多房棘球蚴感染小鼠肝组织结构紊乱、炎性细胞浸润逐渐加重。Masson染色结果显示对照组无明显蓝染区，感染组蓝染面积逐渐增加，感染后15、30、60、90 d蓝染面积占比分别是（22.12 ± 3.09）%、（28.57 ± 2.1）%、（41.20 ± 2.01）%、（58.30 ± 2.21）%（F = 135.60，P < 0.01）。免疫组化染色结果显示IFITM3阳性表达率由对照组（20.18 ± 7.25）%上升至感染后90 d的（56.22 ± 4.49）%（F = 25.40，P < 0.05）；Foxp3阳性表达率由对照组（2.12 ± 1.49）%上升至感染后90 d的（59.10 ± 4.45）%（F = 106.30，P < 0.05）。Western blotting检测结果显示，IFITM3相对表达量在感染后15 d下降至0.27 ± 0.04，随后上升，至感染后90 d达1.01 ± 0.05（F = 52.37，P < 0.05）；Foxp3相对表达量随感染时间延长逐步升高，由对照组的0.03 ± 0.01增加至90 d时的0.97 ± 0.03（F = 143.20，P < 0.05）；二者表达水平呈正相关（R² = 0.687 3，P < 0.05）。ShIFITM3-1、ShIFITM3-2、ShIFITM3-3质粒的转染均使IFITM3相对表达量降低（为0.32 ± 0.02、0.23 ± 0.05、0.53 ± 0.09），其中ShIFITM3-2敲低效率最佳（F = 37.05，P < 0.01）；Foxp3相对表达量随0、0.5、1.0、1.5、2.0 μg的ShIFITM3-2转染后逐渐降低，分别为1.10 ± 0.14、0.62 ± 0.05、0.52 ± 0.04、0.49 ± 0.01、0.33 ± 0.05（F = 42.06，P < 0.01）。分子对接表明，IFITM3与Foxp3的对接评分为-312 kcal/mol，具有良好的亲和作用。免疫共沉淀实验结果表明，IFITM3与Foxp3存在相互作用关系。结论 小鼠多房棘球蚴感染过程中IFITM3与Foxp3存在相互作用关系，二者表达水平与肝组织损伤程度呈正相关。

Objective To investigate the interaction between interferon-inducible transmembrane protein 3 (IFITM3) and forkhead box P3 (Foxp3) in mice during Echinococcus multilocularis infections. Methods E. multilocularis protoscolices were obtained from gerbil liver tissues, and a C57BL/6J mouse model of E. multilocularis infection was established via intraperitoneal injection with E. multilocularis protoscolices. Mice were euthanized 15, 30, 60 and 90 days post-infection, and mouse liver tissues were collected, with uninfected mice as controls. Pathological changes of mouse liver tissues were observed at different time points using hematoxylin-eosin (HE) staining, Masson staining and immunohistochemistry, and the relative expression of IFITM3 and Foxp3 proteins was determined in liver tissues using Western blotting. HEK-293T cells were transfected with IFITM3-ShRNA interference plasmids (ShIFITM3-1, ShIFITM3-2, ShIFITM3-3), and the optimal knockdown fragments were screened for dose-dependent experiments (transfected at 0, 0.5, 1.0, 1.5, 2.0 μg) to further detect changes in Foxp3 expression. The IFITM3-Foxp3 molecular docking was analyzed using the AutoDock software, and the tag plasmid HA-FITTM3 and Flag-Foxp3a were transfected into HEK-293T cells. Total cellular proteins were extracted for immunoprecipitation to verify the interaction between FITTM3 and Foxp3a. Results HE staining revealed disordered arrangements of liver tissues and gradually aggravated infiltration of inflammatory cells in liver tissues of mice infected with E. multilocularis. Masson staining displayed no significant blue staining areas in the control group, and a gradual increase in the blue staining area in the infection group, with (22.12 ± 3.09)%, (28.57 ± 2.1)%, (41.20 ± 2.01)%, and (58.30 ± 2.21)% proportions 15, 30, 60, and 90 days post-infection, respectively (F = 135.60, P < 0.01). Immunohistochemical staining showed that the positive expression rate of IFITM3 increased from (20.18 ± 7.25)% in the control group to (56.22 ± 4.49)% at 90 days post-infection (F = 25.40, P < 0.05), and the positive expression rate of Foxp3 increased from (2.12 ± 1.49)% in the control group to (59.10 ± 4.45)% at 90 days post-infection (F = 106.30, P < 0.05). Western blotting assay showed that the relative expression level of IFITM3 decreased to 0.27 ± 0.04 at 15 days post-infection, and then increased and reached 1.01 ± 0.05 at 90 days post-infection (F = 52.37, P < 0.05), and the relative expression level of Foxp3 gradually increased over time, from 0.03 ± 0.01 in the control group to 0.97 ± 0.03 at 90 days post-infection (F = 143.20, P < 0.05). The IFITM3 expression positively correlated with Foxp3 expression (R² = 0.687 3, P < 0.05). Transfection with ShIFITM3-1, ShIFITM3-2, and ShIFITM3-3 plasmids all resulted in a decrease in the relative expression level of IFITM3 (0.32 ± 0.02, 0.23 ± 0.05, 0.53 ± 0.09), with ShIFITM3-2 showing the highest knockdown efficiency (F = 37.05, P < 0.01), and the relative expression of Foxp3 gradually decreased with ShIFITM3-2 transfection at 0 (1.10 ± 0.14), 0.5 (0.62 ± 0.05), 1.0 (0.52 ± 0.04), 1.5 (0.49 ± 0.01), and 2.0 μg (0.33 ± 0.05), respectively (F = 42.06, P < 0.01). Molecular docking showed that the docking score between IFITM3 and Foxp3 was -312 kcal/mol, indicating a good affinity, and immunoprecipitation indicated an interaction between IFITM3 and Foxp3. Conclusion There is an interaction between IFITM3 and Foxp3 in mice during E. multilocularis infections, and IFITM3 and Foxp3 expression is positively correlated with the severity of liver damages.