Flórido Manuela, Gonçalves Ana Sofia, Gomes M Salomé, Appelberg Rui
Laboratory of Microbiology and Immunology of Infection, Institute for Molecular and Cell Biology, University of Porto, Rua do Campo Alegre 823, 4150-180 Porto, Portugal.
Immunology. 2004 Mar;111(3):323-7. doi: 10.1111/j.1365-2567.2004.01812.x.
C57Bl/6 mice and mice deficient in the CD40 molecule were infected with three strains of Mycobacterium avium. Two of the M. avium strains proliferated more extensively in CD40-deficient (CD40-/-) mice than in control mice. The increased susceptibility to infection of CD40-/- mice was associated with the generation of poorer interleukin-12 (IL-12) p40 and interferon-gamma (IFN-gamma) responses as compared to the controls, suggesting a role for CD40 in the development of protective immunity. In contrast, direct triggering of CD40 on infected macrophages failed to induce any anti-mycobacterial activity in infected macrophages.
将C57Bl/6小鼠和缺乏CD40分子的小鼠用三株鸟分枝杆菌感染。其中两株鸟分枝杆菌在缺乏CD40(CD40-/-)的小鼠中比在对照小鼠中增殖更为广泛。与对照相比,CD40-/-小鼠对感染易感性增加与白细胞介素-12(IL-12)p40和干扰素-γ(IFN-γ)反应较差有关,提示CD40在保护性免疫的发展中起作用。相反,在受感染的巨噬细胞上直接激活CD40未能在受感染的巨噬细胞中诱导任何抗分枝杆菌活性。