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肺炎衣原体感染期间小鼠体内一种新型肺CD3(-) CD4(+) CD8(+)细胞群体的扩增。

Expansion of a novel pulmonary CD3(-) CD4(+) CD8(+) cell population in mice during Chlamydia pneumoniae infection.

作者信息

Penttilä J M, Pyhälä R, Sarvas M, Rautonen N

机构信息

Departments of Vaccines, National Public Health Institute, 00300 Helsinki, Finland.

出版信息

Infect Immun. 1998 Jul;66(7):3290-4. doi: 10.1128/IAI.66.7.3290-3294.1998.

Abstract

A new pulmonary T-cell-like lymphocyte population with the phenotype CD3(-) CD4(+) CD8(+) was discovered in mice. CD4(+) CD8(+) but CD3(+) cells among murine intestinal intraepithelial lymphocytes have previously been described. We describe herein a dramatic expansion of the CD3(-) CD4(+) CD8(+) cell population in response to experimental respiratory infection. After intranasal Chlamydia pneumoniae infection, CD4(+) CD8(+) cells became transiently the dominant lymphocyte type (maximum of 87% of all lymphocytes) in the lungs of NIH/S mice but remained virtually undetectable in spleen and blood. The enrichment of these cells was not a C. pneumoniae-specific event, since infection of NIH/S mice with influenza A virus also resulted in an increase in the number of CD4(+) CD8(+) cells (maximum of 42% of all lymphocytes). In addition to outbred NIH/S mice, two other mouse strains were studied: BALB/c (H-2(d)) and C57BL/6 (H-2(b)). C. pneumoniae-infected BALB/c mice responded with an intermediate increase in the number of CD4(+) CD8(+) cells in lungs, whereas C57BL/6 mice did not respond. The double-positive CD4(+) CD8(+) cells lacked a major part of the T-cell receptor complex, being both CD3(-) and TCR alpha beta-. However, when they were stimulated in vitro with a T-cell mitogen, they responded by proliferation but did not secrete gamma interferon. The dramatic expansion of this cell population at the infection site suggests an active role for them in respiratory infection, but the specification of this requires further study.

摘要

在小鼠中发现了一种新的具有CD3(-) CD4(+) CD8(+)表型的肺T细胞样淋巴细胞群体。此前已描述过小鼠肠道上皮内淋巴细胞中的CD4(+) CD8(+)但CD3(+)细胞。我们在此描述了实验性呼吸道感染后CD3(-) CD4(+) CD8(+)细胞群体的显著扩增。经鼻内感染肺炎衣原体后,CD4(+) CD8(+)细胞在NIH/S小鼠肺中短暂成为主要淋巴细胞类型(最多占所有淋巴细胞的87%),但在脾脏和血液中几乎检测不到。这些细胞的富集并非肺炎衣原体特异性事件,因为用甲型流感病毒感染NIH/S小鼠也导致CD4(+) CD8(+)细胞数量增加(最多占所有淋巴细胞的42%)。除了远交系NIH/S小鼠外,还研究了另外两种小鼠品系:BALB/c(H-2(d))和C57BL/6(H-2(b))。肺炎衣原体感染的BALB/c小鼠肺部CD4(+) CD8(+)细胞数量呈中等程度增加,而C57BL/6小鼠无反应。双阳性CD4(+) CD8(+)细胞缺乏大部分T细胞受体复合物,CD3(-)且TCRαβ-。然而,当它们在体外受到T细胞丝裂原刺激时,会通过增殖做出反应,但不分泌γ干扰素。该细胞群体在感染部位的显著扩增表明它们在呼吸道感染中发挥积极作用,但对此的具体情况还需要进一步研究。

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