Taylor Jennifer L, Ordway Diane J, Troudt Jolynn, Gonzalez-Juarrero Mercedes, Basaraba Randall J, Orme Ian M
Department of Microbiology, Immunology and Pathology, Colorado State University, 200 West Lake Street, 1682 Campus Delivery, Fort Collins, CO 80523-1682, USA.
Infect Immun. 2005 Aug;73(8):5189-93. doi: 10.1128/IAI.73.8.5189-5193.2005.
Resistant C57BL/6 mice infected in the lungs with Mycobacterium tuberculosis and then therapeutically vaccinated with Mycobacterium leprae-derived hsp65 DNA develop severe granulomatous pneumonia and tissue damage. Analysis of cells accumulating in the lungs of these animals revealed substantial increases in T cells secreting tumor necrosis factor alpha and CD8 cells staining positive for granzyme B. Stimulation of lung cells ex vivo revealed very high levels of interleukin-10, some of which was produced by B-1 B cells. This was probably an anti-inflammatory response, since lung pathology was dramatically worsened in B-cell gene-disrupted mice.
对肺部感染结核分枝杆菌的抗性C57BL/6小鼠,随后用源自麻风分枝杆菌的hsp65 DNA进行治疗性疫苗接种,会引发严重的肉芽肿性肺炎和组织损伤。对这些动物肺部积聚细胞的分析显示,分泌肿瘤坏死因子α的T细胞和颗粒酶B染色呈阳性的CD8细胞大幅增加。体外刺激肺细胞显示白细胞介素-10水平非常高,其中一些由B-1 B细胞产生。这可能是一种抗炎反应,因为在B细胞基因敲除小鼠中肺部病理状况显著恶化。