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致敏的CD8 + T细胞无法控制机体负荷,但会加速卡氏肺孢子虫肺炎期间肺损伤的发生。

Sensitized CD8+ T cells fail to control organism burden but accelerate the onset of lung injury during Pneumocystis carinii pneumonia.

作者信息

Gigliotti Francis, Crow Elliott L, Bhagwat Samir P, Wright Terry W

机构信息

Department of Pediatrics, University of Rochester School of Medicine & Dentistry, 601 Elmwood Avenue, Box 690, Rochester, NY 14642, USA.

出版信息

Infect Immun. 2006 Nov;74(11):6310-6. doi: 10.1128/IAI.00668-06. Epub 2006 Aug 28.

Abstract

While CD8+ cells have been shown to contribute to lung injury during Pneumocystis carinii pneumonia (PCP), there are conflicting reports concerning the ability of CD8+ cells to kill P. carinii. To address these two issues, we studied the effect of the presence of CD8+ cells in two mouse models of PCP. In the reconstituted SCID mouse model, depletion of CD8+ cells in addition to CD4+ cells after reconstitution did not result in increased numbers of P. carinii cysts compared to the numbers of cysts in mice with only CD4+ cells depleted. This result was observed regardless of whether the mice were reconstituted with naïve or P. carinii-sensitized lymphocytes. In contrast, reconstitution with sensitized lymphocytes resulted in more rapid onset of lung injury that was dependent on the presence of CD8+ cells. The course of organism replication over a 6-week period was also examined in the CD4+-T-cell-depleted and CD4+- and CD8+-T-cell-depleted mouse model of PCP. Again, the organism burdens were identical at all times regardless of whether CD8+ cells were present. Thus, in the absence of CD4+ T cells, CD8+ T cells are a key contributor to the inflammatory lung injury associated with PCP. However, we were unable to demonstrate an in vivo effect of these cells on the course of P. carinii infection.

摘要

虽然已表明CD8 +细胞在卡氏肺孢子虫肺炎(PCP)期间对肺损伤有影响,但关于CD8 +细胞杀死卡氏肺孢子虫的能力存在相互矛盾的报道。为了解决这两个问题,我们在两种PCP小鼠模型中研究了CD8 +细胞存在的影响。在重建的SCID小鼠模型中,重建后除了CD4 +细胞外耗尽CD8 +细胞,与仅耗尽CD4 +细胞的小鼠相比,并未导致卡氏肺孢子虫囊肿数量增加。无论小鼠是用未致敏的还是对卡氏肺孢子虫致敏的淋巴细胞重建,都观察到了这一结果。相反,用致敏淋巴细胞重建导致肺损伤的发作更快,这取决于CD8 +细胞的存在。在PCP的CD4 + T细胞耗尽和CD4 +和CD8 + T细胞耗尽的小鼠模型中,还检查了6周内生物体复制的过程。同样,无论是否存在CD8 +细胞,生物体负担在所有时间都是相同的。因此,在没有CD4 + T细胞的情况下,CD8 + T细胞是与PCP相关的炎症性肺损伤的关键因素。然而,我们无法证明这些细胞对卡氏肺孢子虫感染过程的体内作用。

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