Magee D M, Williams D M, Smith J G, Bleicker C A, Grubbs B G, Schachter J, Rank R G
Department of Research Immunology, Texas Center for Infectious Disease, San Antonio 78223.
Infect Immun. 1995 Feb;63(2):516-21. doi: 10.1128/iai.63.2.516-521.1995.
The role of CD4 and CD8 T cells in primary Chlamydia trachomatis pneumonia was investigated by using in vivo depletion techniques to eliminate T-cell populations. Reduction of either CD4 T cells or CD8 T cells caused a significant increase in organism burden in the lungs, as measured by both quantitative culture and detection of chlamydial antigen on day 14 postinfection. Chlamydia-specific antibody levels in plasma or antigen-induced gamma interferon (IFN-gamma) production by spleen cells was dramatically reduced by depletion of CD4 cells. The reduction in IFN-gamma achieved by depletion of CD8 cells did not reach statistical significance. In the survival studies, depletion of CD4 cells led to a significant increase in mortality. Although there was a trend toward higher mortality, depletion of CD8 cells did not significantly increase mortality. The role of CD8 T cells in host defense was clarified in studies using beta 2-microglobulin-deficient (major histocompatibility class I antigen-deficient, C1D) mice which are defective in CD8 T-cell function. In this model, a significant increase in organism burden was seen during infection in C1D mice compared with that C57BL/6 controls and a significant increase in mortality was observed as well. However, surviving C1D mice were able to clear the infection by day 34. C1D mice had increased numbers of CD4 T cells in both the spleen and the lungs during infection compared with those of C57BL/6 controls. IFN-gamma in C57BL/6 mice was produced by both CD4 and CD8 cells. Thus, there is a protective role for both CD4 and CD8 cells in host defense against Chlamydia infection, but the former appear to be dominant.
通过运用体内清除技术去除T细胞群体,研究了CD4和CD8 T细胞在原发性沙眼衣原体肺炎中的作用。在感染后第14天,通过定量培养和衣原体抗原检测发现,CD4 T细胞或CD8 T细胞的减少均导致肺部病原体负荷显著增加。CD4细胞的清除显著降低了血浆中衣原体特异性抗体水平或脾细胞抗原诱导的γ干扰素(IFN-γ)产生。CD8细胞清除导致的IFN-γ减少未达到统计学意义。在生存研究中,CD4细胞的清除导致死亡率显著增加。虽然CD8细胞的清除有导致更高死亡率的趋势,但未显著增加死亡率。在使用β2-微球蛋白缺陷(主要组织相容性复合体I类抗原缺陷,C1D)小鼠的研究中阐明了CD8 T细胞在宿主防御中的作用,这类小鼠的CD8 T细胞功能存在缺陷。在该模型中,与C57BL/6对照小鼠相比,C1D小鼠在感染期间病原体负荷显著增加,死亡率也显著升高。然而,存活的C1D小鼠在感染后34天能够清除感染。与C57BL/6对照小鼠相比,C1D小鼠在感染期间脾脏和肺部的CD4 T细胞数量增加。C57BL/6小鼠中的IFN-γ由CD4和CD8细胞产生。因此,CD4和CD8细胞在宿主防御衣原体感染中均起保护作用,但前者似乎占主导地位。