Role of NK1.1+ cells in experimental listeriosis. NK1+ cells are early IFN-gamma producers but impair resistance to Listeria monocytogenes infection.
Role of NK1.1+ cells in experimental listeriosis. NK1+ cells are early IFN-gamma producers but impair resistance to Listeria monocytogenes infection.
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DOI：
10.4049/jimmunol.152.4.1873
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发表时间：
1994-02
影响因子：
4.4
通讯作者：
H. Teixeira;S. Kaufmann
中科院分区：
文献类型：
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作者：
H. Teixeira;S. Kaufmann
采用酶联免疫斑点法检测C57Bl/6和BALB/c小鼠脾脏ifn - γ和IL-4斑点形成细胞，这两种小鼠对系统性单核细胞增生乳杆菌感染的抗性不同。感染后第1天、第7天和第14天，C57Bl/6小鼠自发性和Ag（热杀李斯特菌）诱导的ifn - γ SFC数量比BALB/c小鼠高5- 10倍。在这两种小鼠中，ag诱导的ifn - γ产生在感染后第7天达到最高水平，IL-4产生在第1天略有增加，此后下降。体外和体内用PK136单克隆抗体消耗NK1+细胞可以消除C57Bl/6小鼠的早期ifn - γ产生（第1天），这表明NK1+细胞在感染后第1天是主要的ifn - γ产生细胞。体内消耗NK1+细胞可显著增加C57Bl/6小鼠脾脏中IL-4斑点形成细胞的数量，提示NK1+细胞和ifn - γ对IL-4的产生有调节作用。感染后第5天，C57Bl/6小鼠脾脏细菌数量高于BALB/c小鼠。抗nk1.1单抗治疗和11B11单抗在体内中和IL-4可增强C57Bl/6小鼠的细胞清除能力。这些结果表明：1)BALB/c小鼠比C57Bl/6小鼠对单核增生乳杆菌EGD感染的抗性更强；2)NK1+细胞和IL-4在单核增生乳杆菌感染中起不利作用；3)抗李斯特菌抗性和ifn - γ水平是可分离的。
An enzyme-linked immunospot assay was used for detection of splenic IFN-gamma and IL-4 spot-forming cells from, C57Bl/6 and BALB/c mice, which differ in resistance to systemic L. monocytogenes infection. Numbers of spontaneous and Ag (heat-killed listeriae)-induced IFN-gamma SFC were 5- to 10-fold higher in C57Bl/6 as compared to BALB/c mice at day 1, day 7, and day 14 postinfection. In both strains of mice, Ag-induced IFN-gamma production reached maximum levels at day 7 postinfection and IL-4 production was slightly increased at day 1, decreasing thereafter. The early IFN-gamma production (day 1) in C57Bl/6 mice was abrogated by in vitro and in vivo depletion of NK1+ cells with PK136 mAbs, indicating that NK1+ cells are major IFN-gamma producers at day 1 after infection. In vivo depletion of NK1+ cells markedly increased numbers of IL-4 spot-forming cells in spleens of C57Bl/6 mice, suggesting a modulatory effect of NK1+ cells and IFN-gamma on IL-4 production. At day 5 postinfection, bacterial numbers in spleens were higher in C57Bl/6 than in BALB/c mice. Treatment with the anti-NK1.1 mAb and in vivo neutralization of IL-4 with the 11B11 mAb enhanced listerial clearing in C57Bl/6 mice. These findings suggest 1) BALB/c mice are more resistant than C57Bl/6 mice to L. monocytogenes EGD infection, 2) NK1+ cells and IL-4 play a detrimental role in L. monocytogenes infection, and 3) antilisterial resistance and levels of IFN-gamma are dissociable.