Hamada Satoru, Umemura Masayuki, Shiono Takeru, Hara Hiromitsu, Kishihara Kenji, Tanaka Kensho, Mayuzumi Hirokazu, Ohta Takao, Matsuzaki Goro
Molecular Microbiology Group, Centre of Molecular Biosciences, University of the Ryukyus, Okinawa, Japan.
Immunology. 2008 Oct;125(2):170-7. doi: 10.1111/j.1365-2567.2008.02841.x. Epub 2008 Apr 7.
Murine gammadelta T cells participate in the innate immune response against infection by an intracellular pathogen Listeria monocytogenes. Vdelta1+gammadelta T cells coexpressing Vgamma6 are a major gammadelta T-cell subpopulation induced at an early stage of L. monocytogenes infection in the livers of infected mice. To investigate the protective role of the Vgamma6/Vdelta1+gammadelta T cells against L. monocytogenes infection, Vdelta1 gene-deficient (Vdelta1-/-) mice were analysed because these mice selectively lacked a Vgamma6/Vdelta1+gammadelta T-cell subpopulation in the L. monocytogenes-infected liver. The Vdelta1-/- mice showed increased bacterial burden in the liver and spleen, and decreased survival rate at an early stage of L. monocytogenes infection when compared to wild-type mice. Histological examination showed abscess-like lesions and unorganized distribution of macrophages in the liver of the Vdelta1-/- mice but not in the wild-type mice after L. monocytogenes infection. The Vgamma6/Vdelta1+gammadelta T cells produced interferon-gamma and interleukin-17A. All the results suggest that murine Vgamma6/Vdelta1+gammadelta T cells control the innate protective response against L. monocytogenes infection through production of the proinflammatory cytokines interferon-gamma and interleukin-17A in the infected liver.
小鼠γδ T细胞参与针对细胞内病原体单核细胞增生李斯特菌感染的固有免疫反应。共表达Vγ6的Vδ1⁺γδ T细胞是感染小鼠肝脏中在单核细胞增生李斯特菌感染早期诱导产生的主要γδ T细胞亚群。为了研究Vγ6/Vδ1⁺γδ T细胞对单核细胞增生李斯特菌感染的保护作用，对Vδ1基因缺陷（Vδ1⁻/⁻）小鼠进行了分析，因为这些小鼠在单核细胞增生李斯特菌感染的肝脏中选择性地缺乏Vγ6/Vδ1⁺γδ T细胞亚群。与野生型小鼠相比，Vδ1⁻/⁻小鼠在单核细胞增生李斯特菌感染早期肝脏和脾脏中的细菌负荷增加，存活率降低。组织学检查显示，单核细胞增生李斯特菌感染后，Vδ1⁻/⁻小鼠肝脏中有脓肿样病变且巨噬细胞分布无序，而野生型小鼠则没有。Vγ6/Vδ1⁺γδ T细胞产生干扰素-γ和白细胞介素-17A。所有结果表明，小鼠Vγ6/Vδ1⁺γδ T细胞通过在感染的肝脏中产生促炎细胞因子干扰素-γ和白细胞介素-17A来控制针对单核细胞增生李斯特菌感染的固有保护反应。
