Titus R G, DeKrey G K, Morris R V, Soares M B
Departments of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado 80523-1671, USA.
Infect Immun. 2001 Aug;69(8):5189-92. doi: 10.1128/IAI.69.8.5189-5192.2001.
Since interleukin-6 (IL-6) may promote Th2 responses, we infected BALB IL-6-deficient (IL-6(-/-)) mice with Leishmania major. There was not a significant difference between the courses of infection (lesion size and parasite burden) in IL-6(-/-) and wild-type mice, but IL-6(-/-) mice expressed lower levels of Th2- and Th1-associated cytokines.
由于白细胞介素-6(IL-6)可能促进Th2反应,我们用硕大利什曼原虫感染了BALB IL-6缺陷(IL-6(-/-))小鼠。IL-6(-/-)小鼠和野生型小鼠在感染过程(病变大小和寄生虫负荷)上没有显著差异,但IL-6(-/-)小鼠表达的Th2和Th1相关细胞因子水平较低。