Depletion of CD8+ T cells exacerbates CD4+ Th cell-associated inflammatory lesions during murine mycoplasma respiratory disease
Depletion of CD8+ T cells exacerbates CD4+ Th cell-associated inflammatory lesions during murine mycoplasma respiratory disease
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DOI：
10.4049/jimmunol.168.7.3493
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发表时间：
2002-04-01
影响因子：
4.4
通讯作者：
Simecka, JW
中科院分区：
文献类型：
--
作者：
Jones, HP;Tabor, L;Simecka, JW
支原体感染是全球肺炎的主要原因，并可导致其他呼吸道并发症。支原体呼吸道疾病的一个组成部分是免疫病理学的，这表明淋巴细胞活化是这些慢性炎性疾病进展中的关键事件。本研究描述了T细胞群的变化和支原体感染后的激活，并确定其与小鼠支原体呼吸道疾病的发病机制，由于肺支原体感染。肺和下呼吸道淋巴结中T细胞群数量的增加与支原体呼吸道疾病的发生相关。虽然支原体感染后肺Th和CD 8（+）T细胞均增加，但Th细胞优先扩增。支原体特异性Th 2反应在下呼吸道淋巴结中占主导地位，而Th 1反应在脾脏中占主导地位。然而，支原体特异性Th 1和Th 2细胞因子（IL-4和IFN-γ）反应都存在于肺中，Th 1细胞活化是肺Th细胞反应的主要组成部分。尽管支原体特异性CD 8（+）T细胞是T细胞应答的一个较小组成部分，但它也是肺淋巴应答的重要组成部分。体内CD 8（+）T细胞耗竭导致肺部疾病的严重程度显著增加，而CD 4（+）T细胞耗竭降低了其严重程度，但细胞耗竭后肺部支原体数量没有变化。因此，肺中支原体特异性Th 1和CD 8（+）T细胞活化在支原体呼吸道疾病免疫病理反应的发展中起着关键的调节作用。
Mycoplasma infection is a leading cause of pneumonia worldwide and can lead to other respiratory complications. A component of mycoplasma respiratory diseases is immunopathologic, suggesting that lymphocyte activation is a key event in the progression of these chronic inflammatory diseases. The present study delineates the changes in T cell populations and their activation after mycoplasma infection and determines their association with the pathogenesis of murine Mycoplasma respiratory disease, due to Mycoplasma pulmonis infection. Increases in T cell population numbers in lungs and lower respiratory lymph nodes were associated with the development of mycoplasma respiratory disease. Although both pulmonary Th and CD8(+) T cells increased after mycoplasma infection, there was a preferential expansion of Th cells. Mycoplasma-specific Th2 responses were dominant in lower respiratory lymph nodes, while Th1 responses predominated in spleen. However, both mycoplasma-specific Th1 and Th2 cytokine (IL-4 and IFN-gamma) responses were present in the lungs, with Th1 cell activation as a major component of the pulmonary Th cell response. Although a smaller component of the T cell response, mycoplasma-specific CD8(+) T cells were also a significant component of pulmonary lymphoid responses. In vivo depletion of CD8(+) T cells resulted in dramatically more severe pulmonary disease, while depletion of CD4(+) T cells reduced its severity, but there was no change in mycoplasma numbers in lungs after cell depletion. Thus, mycoplasma-specific Th1 and CD8(+) T cell activation in the lung plays a critical regulatory role in development of immunopathologic reactions in Mycoplasma respiratory disease.