CD8~+ T细胞在CD4~+ T细胞耗竭小鼠卡氏肺孢子虫肺炎的致病作用

[目的 ]验证参与卡氏肺孢子虫致病过程中 ,宿主炎性反应及其对肺功能的影响。 [方法 ]:将小鼠CD4+ T细胞耗竭或将小鼠CD4+ 和CD8+ T细胞都耗竭后 ,经气管接种卡氏肺孢子虫。观察在CD8+ T细胞缺如或存在的情况下 ,小鼠呼吸机能的改变和肺炎的程度。 [结果 ]耗竭CD4+ 和CD8+ T细胞后 ,小鼠虽发生PCP ,但呼吸频率无明显加快 ,肺组织损伤程度也较轻。相反 ,仅耗竭CD4+ T细胞保留CD8+ T细胞的小鼠的呼吸频率明显加快 ,肺内炎性细胞反应和肺组织损伤程度均较重。支气管肺泡灌洗液 (BALF)中的CD8+ T细胞和嗜中性白细胞的数量明显增多。 [结论 ]PCP的致病过程中 ,宿主的炎性细胞反应对肺功能有直接损伤作用 ,其中CD8+ T细胞似起主要作用。

THE ROLE OF CD8+ T CELLS IN THE PATHOGENESIS OF PNEUMOCYSTIS CARINII PNEUMONIA IN MICE DEPLETED OF CD4+ T CELLS

OBJECTIVE: To define the cell populations contributing to inflammation-associated respiratory impairment in Pneumocystis carinii pneumonia (PCP). METHODS: The host inflammation response was observed in CD4+ T cell-depleted mice and in CD4+ and CD8+ T cell-depleted mice infected with P. carinii via intratracheal inoculation. RESULTS: Mice depleted of both CD4+ and CD8+ T cells developed infection with neither increased respiratory rate nor lung injury. In contrast, mice depleted of CD4+ T cells alone exhibited severe pulmonary inflammation, and increased respiratory rates. Respiratory compromise was associated with the presence of activated CD8+ cells and neutrophils in the BALF. CONCLUSION: The host's inflammatory cell response to P. carinii directly impairs pulmonary function and contributes to the pathogenesis of PCP, CD8+ T cells appear to play a major role.