Temporal development of protective cell-mediated and humoral immunity in BALB/c mice infected with Brucella abortus.
Temporal development of protective cell-mediated and humoral immunity in BALB/c mice infected with Brucella abortus.
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DOI：
10.4049/jimmunol.143.10.3330
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发表时间：
1989-11
影响因子：
4.4
通讯作者：
L. Araya;P. Elzer;G. Rowe;F. Enright;A. Winter
中科院分区：
文献类型：
--
作者：
L. Araya;P. Elzer;G. Rowe;F. Enright;A. Winter
在静脉感染的BALB/c小鼠中。布鲁氏菌减毒株19在脾内大量复制，在感染后2周达到高峰。然后逐步清除感染，以便在8周前P.I.细菌数量减少了10,000倍或更多。对感染前2周、3周、4周、5周、6周和8周的供体小鼠进行T细胞浓缩的脾细胞和血清被动移植试验。抗体在免疫后3wk对受者有显著的保护作用，而T细胞的保护作用直到4wk才明显。当在攻击感染之前而不是在攻击感染之后进行转移时，血清和细胞的联合转移比血清或细胞单独提供的保护更强。来自6周捐赠者的富含T细胞的脾细胞所提供的保护不受相同数量的3周捐赠者的细胞的影响，但由于去除了CD4和CD8 T细胞亚群而被取消。对纯化的CD4和CD8亚群的实验表明，细胞介导的保护在这两个亚群中处于同等水平。感染后每天给予环孢素A 4wk，可引起小鼠脾、肝内布鲁氏菌数量增加。虽然治疗组动物的免疫反应明显受到抑制，但对脾内巨噬细胞的数量、对脾内单核细胞增生性李斯特菌的杀灭作用以及对脾和肝脏炎症反应的性质和强度影响不大。这些数据表明，小鼠对流产杆菌感染的获得性抵抗力是CD4和CD8表型抗体和T效应细胞的独立作用的结果，可能也是相互作用的结果。脾中细菌数量最初的下降是在该器官中没有可检测到的细胞免疫的情况下发生的，可能主要归因于抗体的影响和非免疫刺激对巨噬细胞的形成、吸引和激活的增加。
In BALB/c mice infected i.v. with attenuated strain 19 of Brucella abortus, the organism replicates to high numbers in the spleen and reaches peak concentrations at 2 wk postinfection (p.i.). The infection is then progressively cleared so that by 8 wk p.i. numbers of bacteria have decreased 10,000 fold or more. Passive transfer assays were performed with T cell-enriched spleen cells and serum of donor mice infected 2, 3, 4, 5, 6, or 8 wk previously. Antibodies conferred significant protection to recipients at and after 3 wk p.i., whereas protection by T cells was not evident until 4 wk p.i. The combined transfer of serum and cells enhanced protection over that provided by serum or cells alone when transfers were made before, but not after, challenge infection. Protection conferred by T cell-enriched spleen cells of 6-wk donors was unaffected by the presence of equal quantities of cells from 3-wk donors, but was abrogated by the removal of both CD4 and CD8 T cell subsets. Experiments with purified CD4 and CD8 subsets revealed that cell-mediated protection resided at equivalent levels in both subsets. Daily treatment of mice with Cyclosporin A for 4 wk after infection caused some increase in numbers of brucellae in spleens and livers. Although immune responses of treated animals were markedly suppressed, there was little effect of treatment on numbers of macrophages in the spleen, on enhanced killing of Listeria monocytogenes in the spleen, or on the nature and intensity of splenic and hepatic inflammatory responses. These data indicate that acquired resistance to infection with B. abortus in mice is the result of independent, and probably also interactive, effects of antibodies and T effector cells of both CD4 and CD8 phenotypes. The initial decline in bacterial numbers in the spleen, which occurred in the absence of detectable cell-mediated immunity in that organ, could probably be ascribed principally to effects of antibodies and to nonimmune stimuli responsible for increased formation, attraction, and activation of macrophages.