Department of Microbiology and Immunology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Parasite Immunol. 2009 Dec;31(12):741-9. doi: 10.1111/j.1365-3024.2009.01151.x.
Protection against Mesocestoides corti, a cestode that invades vital organs, is dependent on the production of IL-4, as IL-4(-/-) mice were found to have higher parasite burdens when compared with wild-type mice. The goal of this study was to investigate the role of IL-4 in immunity to M. corti, focusing on the immunological profile and on potential mediators of pathology. IL-4(-/-) mice infected with M. corti showed 100% mortality by 32 days, whereas wild-type mice survived for approximately 1 year. Parasite burdens were significantly increased in the liver, peritoneal, and thoracic cavities of IL-4(-/-) mice, associated with impaired recruitment of inflammatory cells and a reduction in monocytes and macrophages. IL-5 production by splenocytes and expression in liver tissue was decreased in infected IL-4(-/-) mice compared with wild-type mice. In contrast, IL-4(-/-) mice produced increased amounts of IFNgamma and TNFalpha. Alternatively activated macrophages were a major feature of liver granulomas in wild-type mice evidenced by Arginase I expression, while livers from infected IL-4(-/-) mice showed impaired alternative macrophage activation without increased classical macrophage activation. Thus, lethality during M. corti infection of IL-4(-/-) mice is associated with decreased Th2 cytokines, increased Th1 cytokines and impairment of alternatively activated macrophages.
针对侵袭重要器官的中殖孔绦虫(Mesocestoides corti)的保护作用依赖于 IL-4 的产生,因为与野生型小鼠相比,IL-4(-/-)小鼠的寄生虫负担更高。本研究的目的是研究 IL-4 在抗 M. corti 免疫中的作用,重点关注免疫谱和潜在的病理学介质。感染 M. corti 的 IL-4(-/-)小鼠在 32 天内死亡率达到 100%,而野生型小鼠可存活约 1 年。IL-4(-/-)小鼠肝脏、腹膜腔和胸腔中的寄生虫负担显著增加,与炎症细胞募集受损以及单核细胞和巨噬细胞减少有关。与野生型小鼠相比,感染的 IL-4(-/-)小鼠脾细胞产生的 IL-5 减少,肝组织中表达的 IL-5 减少。相比之下,IL-4(-/-)小鼠产生的 IFNγ和 TNFα 增加。在野生型小鼠的肝脏肉芽肿中,替代激活的巨噬细胞是一个主要特征,表现为精氨酸酶 I 的表达,而感染的 IL-4(-/-)小鼠的肝脏显示替代巨噬细胞激活受损,而经典巨噬细胞激活没有增加。因此,IL-4(-/-)小鼠在感染 M. corti 时的致死性与 Th2 细胞因子减少、Th1 细胞因子增加和替代激活的巨噬细胞受损有关。