Vester B, Müller K, Solbach W, Laskay T
Institute for Clinical Microbiology and Immunology, University of Erlangen-Nürnberg, Erlangen, Germany.
Infect Immun. 1999 Jun;67(6):3155-9. doi: 10.1128/IAI.67.6.3155-3159.1999.
Susceptibility of mice to Leishmania major is associated with an insufficient NK cell-mediated innate immune response. We analyzed the expression of NK cell-activating chemokines in vivo during the first days of infection in resistant and susceptible mice. The mRNA expression of gamma interferon-inducible protein 10 (IP-10), monocyte chemoattractant protein 1 (MCP-1), and lymphotactin was upregulated 1 day after infection in the draining lymph nodes of resistant C57BL/6 mice but not in those of susceptible BALB/c mice. In vivo local treatment of BALB/c mice with recombinant IP-10 shortly after infection resulted in an enhanced NK cell activity in the draining lymph node. The data suggest that although the recruitment of NK cells is normal in susceptible mice, the lack of NK cell-activating chemokines is a factor resulting in a suboptimal NK cell-mediated defense.
小鼠对硕大利什曼原虫的易感性与自然杀伤细胞(NK细胞)介导的先天性免疫反应不足有关。我们分析了在感染的最初几天里,抗性和易感小鼠体内NK细胞激活趋化因子的表达情况。感染后1天,抗性C57BL/6小鼠引流淋巴结中γ干扰素诱导蛋白10(IP-10)、单核细胞趋化蛋白1(MCP-1)和淋巴细胞趋化因子的mRNA表达上调,而易感BALB/c小鼠的则未上调。感染后不久对BALB/c小鼠进行重组IP-10的体内局部治疗,导致引流淋巴结中NK细胞活性增强。数据表明,虽然易感小鼠中NK细胞的募集正常,但缺乏NK细胞激活趋化因子是导致NK细胞介导的防御作用欠佳的一个因素。