Usami J, Hiromatsu K, Matsumoto Y, Maeda K, Inagaki H, Suzuki T, Yoshikai Y
Department of Internal Medicine, Nagoya University Branch Hospital, Japan.
Immunology. 1995 Oct;86(2):199-205.
We investigated the host defense mechanism in primary infection with Listeria monocytogenes in non-obese diabetic (NOD) mice at pre-diabetic stage showing an impaired responsiveness of the alpha beta T cells to T-cell receptor (TCR) triggering. The NOD mice showed a deteriorated resistance at the late stage after an intraperitoneal infection with L. monocytogenes compared with BALB/c and C57BL/6 mice as assessed by bacterial growth in organs. Consistent with our previous findings, a prominent increase in number of gamma delta T cells was evident at the early stage after infection, while generation of Listeria-specific alpha beta T cells was impaired in these mice. In vivo administration of anti-TCR gamma delta monoclonal antibody (mAb) allowed L. monocytogenes to grow exaggeratedly in the NOD mice. These results imply that gamma delta T cells may be mainly involved in protection against primary infection with L. monocytogenes in NOD mice.
我们研究了非肥胖糖尿病(NOD)小鼠在糖尿病前期原发性单核细胞增生李斯特菌感染中的宿主防御机制,这些小鼠的αβ T细胞对T细胞受体(TCR)触发的反应性受损。通过器官中的细菌生长评估,与BALB/c和C57BL/6小鼠相比,NOD小鼠在腹腔感染单核细胞增生李斯特菌后的后期抵抗力下降。与我们之前的发现一致,感染后早期γδ T细胞数量显著增加,而这些小鼠中李斯特菌特异性αβ T细胞的生成受损。体内给予抗TCRγδ单克隆抗体(mAb)使单核细胞增生李斯特菌在NOD小鼠中过度生长。这些结果表明,γδ T细胞可能主要参与NOD小鼠抵御原发性单核细胞增生李斯特菌感染的过程。