Matsuzaki Goro, Yamada Hisakata, Kishihara Kenji, Yoshikai Yasunobu, Nomoto Kikuo
Department of Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Eur J Immunol. 2002 Apr;32(4):928-35. doi: 10.1002/1521-4141(200204)32:4<928::AID-IMMU928>3.0.CO;2-I.
Murine gamma delta T cells participate in innate immune response against infection of the intracellular bacterium Listeria monocytogenes. In the present report, we analyzed the mechanism of the gamma delta T cell-mediated response against L. monocytogenes infection. gamma delta T cell-enriched spleen cells of L. monocytogenes-infected mice produced IFN-gamma in vitro in response to L. monocytogenes-infected spleen cells. The IFN-gamma production was abrogated by depletion of Vgamma1+ gamma delta T cells. IFN-gamma production of the Vgamma1+ gamma delta T cells in response to L. monocytogenes-infected spleen cells required IL-12. However, addition of Fab fragment of anti-TCR gamma delta monoclonal antibodies (mAb) failed to block the response, suggesting that the response requires no TCR-mediated antigen recognition. Interestingly, Vgamma1+ gamma delta T cells of naive mice also produced IFN-gamma in response to L. monocytogenes-infected spleen cells in an IL-12-dependent manner. Furthermore, the IL-12 receptor (IL-12R) gene was expressed on the Vgamma1+ gamma delta T cells of naive mice as well as those of L. monocytogenes-infected mice although naive alpha beta T cells lack IL-12R expression. All the results suggest that the Vgamma1+ gamma delta T cells participate in immune surveillance against intracellular bacterial infection through quick production of IFN-gamma in response to infection-induced IL-12 without antigen-driven clonal expansion and maturation.
小鼠γδ T细胞参与针对细胞内细菌单核细胞增生李斯特菌感染的先天免疫反应。在本报告中，我们分析了γδ T细胞介导的针对单核细胞增生李斯特菌感染的反应机制。单核细胞增生李斯特菌感染小鼠的富含γδ T细胞的脾细胞在体外对单核细胞增生李斯特菌感染的脾细胞产生干扰素-γ。Vγ1⁺γδ T细胞的耗竭消除了干扰素-γ的产生。Vγ1⁺γδ T细胞对单核细胞增生李斯特菌感染的脾细胞产生干扰素-γ需要白细胞介素-12。然而，添加抗TCRγδ单克隆抗体（mAb）的Fab片段未能阻断该反应，这表明该反应不需要TCR介导的抗原识别。有趣的是，未感染小鼠的Vγ1⁺γδ T细胞也以白细胞介素-12依赖的方式对单核细胞增生李斯特菌感染的脾细胞产生干扰素-γ。此外，白细胞介素-12受体（IL-12R）基因在未感染小鼠以及单核细胞增生李斯特菌感染小鼠的Vγ1⁺γδ T细胞上表达，尽管未感染的αβ T细胞缺乏IL-12R表达。所有结果表明，Vγ1⁺γδ T细胞通过在感染诱导的白细胞介素-12作用下快速产生干扰素-γ来参与针对细胞内细菌感染的免疫监视，而无需抗原驱动的克隆扩增和成熟。
