Gautreaux M D, Deitch E A, Berg R D
Department of Microbiology and Immunology, Louisiana State University Medical Center, Shreveport 71130-3932.
Infect Immun. 1994 Jul;62(7):2874-84. doi: 10.1128/iai.62.7.2874-2884.1994.
Flow cytofluorometric analyses of lymphocytes harvested from the mesenteric lymph node (MLN), mucosal epithelium, and lamina propria of C57BL/6 mice demonstrate that expression of alpha/beta or gamma/delta T-cell receptors (TCR) and CD4 or CD8 molecules by T lymphocytes in the intestinal immune system varies depending upon their anatomic location. The MLN contained equivalent numbers of CD4+ and CD8+ T cells, the vast majority of which were alpha/beta TCR positive (alpha/beta TCR+). The lamina propria T cells were predominantly CD4+ and alpha/beta TCR+, while the intestinal intraepithelial lymphocytes consisted of equivalent numbers of alpha/beta and gamma/delta T cells, the majority of which were CD8+. There were no significant changes in these T-cell phenotypic profiles when the mice were antibiotic decontaminated or monoassociated with Escherichia coli. Mice were depleted of CD4+ T cells and/or CD8+ T cells in vivo by intraperitoneal injections of monoclonal antibody GK 1.5 (rat anti-mouse CD4) and/or monoclonal antibody 2.43 (rat anti-mouse CD8). T-cell depletion was confirmed in the MLN, lamina propria, and the intestinal epithelium by flow cytometry. E. coli C25 translocation from the gastrointestinal (GI) tract to the MLN was significantly increased in mice depleted of CD4+ T cells, CD8+ T cells, or both. T-cell-deficient athymic beige/nude mice also exhibited greater levels of E. coli C25 translocation to the MLN than beige/het euthymic littermates. Salmonella typhimurium translocation also was increased following CD4+ and CD8+ T-cell depletion in mice monoassociated with S. typhimurium. Depletion of CD4+ and/or CD8+ T cells also increased the translocation to the MLN of certain indigenous GI flora bacteria. These results confirm that T-cell-mediated immunity is involved in the host defense against bacterial translocation from the GI tract.
对从C57BL/6小鼠肠系膜淋巴结（MLN）、黏膜上皮和固有层采集的淋巴细胞进行流式细胞荧光分析表明，肠道免疫系统中T淋巴细胞的α/β或γ/δ T细胞受体（TCR）以及CD4或CD8分子的表达因其解剖位置而异。MLN中CD4⁺和CD8⁺ T细胞数量相当，其中绝大多数为α/β TCR阳性（α/β TCR⁺）。固有层T细胞主要为CD4⁺和α/β TCR⁺，而肠道上皮内淋巴细胞由数量相当的α/β和γ/δ T细胞组成，其中大多数为CD8⁺。当小鼠接受抗生素去污或与大肠杆菌单联时，这些T细胞表型谱没有显著变化。通过腹腔注射单克隆抗体GK 1.5（大鼠抗小鼠CD4）和/或单克隆抗体2.43（大鼠抗小鼠CD8）在体内使小鼠的CD4⁺ T细胞和/或CD8⁺ T细胞耗竭。通过流式细胞术在MLN、固有层和肠道上皮中证实了T细胞耗竭。在CD4⁺ T细胞、CD8⁺ T细胞或两者均耗竭的小鼠中，大肠杆菌C25从胃肠道（GI）向MLN的易位显著增加。T细胞缺陷的无胸腺米色/裸鼠向MLN的大肠杆菌C25易位水平也高于有胸腺的米色/杂合同窝小鼠。在与鼠伤寒沙门氏菌单联的小鼠中，CD4⁺和CD8⁺ T细胞耗竭后，鼠伤寒沙门氏菌的易位也增加了。CD4⁺和/或CD8⁺ T细胞的耗竭还增加了某些肠道固有菌群细菌向MLN的易位。这些结果证实，T细胞介导的免疫参与宿主抵御细菌从胃肠道易位的防御过程。
