CD4(+) AND CD8(+) T-CELL-DEPENDENT AND T-CELL-INDEPENDENT HOST-DEFENSE MECHANISMS CAN OPERATE TO CONTROL AND RESOLVE PRIMARY AND SECONDARY FRANCISELLA-TULARENSIS LVS INFECTION IN MICE
CD4(+) AND CD8(+) T-CELL-DEPENDENT AND T-CELL-INDEPENDENT HOST-DEFENSE MECHANISMS CAN OPERATE TO CONTROL AND RESOLVE PRIMARY AND SECONDARY FRANCISELLA-TULARENSIS LVS INFECTION IN MICE
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DOI：
10.1128/iai.62.12.5603-5607.1994
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发表时间：
1994-12-01
影响因子：
3.1
通讯作者：
NORTH, RJ
中科院分区：
文献类型：
--
作者：
CONLAN, JW;SJOSTEDT, A;NORTH, RJ
对兼性细胞内细菌Francisella tularensis的实验感染免疫通常被认为是T细胞介导的巨噬细胞表达的免疫的例子。然而，本研究的结果表明，T细胞非依赖机制在抗链球菌防御中也很重要。他们表明，通过T细胞亚群特异性单抗治疗而选择性地耗尽了CD4(+)、CD8(+)或两者兼而有之的小鼠，仍然能够控制和部分消除原发的亚致死性方济氏菌感染。类似地，研究发现，缺失其中一种或两种T细胞亚群的弗朗西塞拉免疫小鼠对再次感染保持了高度的获得性免疫力。综上所述，这些发现表明，对初发和继发性兔热病的抵抗可以由CD4(+)和CD8(+)T细胞以外的细胞介导。
Immunity to experimental infection with the facultative intracellular bacterium Francisella tularensis is generally considered an example of T-cell-mediated, macrophage-expressed immunity. However, the results of the present study indicate that T-cell-independent mechanisms are also important in anti-Francisella defense. They show that mice selectively depleted of CD4(+), CD8(+), or both T-cell populations by treatment with T-cell subset-specific monoclonal antibodies remained capable of controlling and partly resolving a primary sublethal Francisella infection. Similarly, it was found that Francisella-immune mice depleted of either or both subsets of T cells retain a high degree of acquired immunity to reinfection. Together, these findings imply that resistance to primacy and secondary tularemia can be mediated by cells other than CD4(+) and CD8(+) T cells.