Chang J C, Distler S G, Kaplan A M
Department of Microbiology and Immunology, University of Kentucky Medical Center, Lexington 40536-0084.
Toxicol Appl Pharmacol. 1990 Mar 1;102(3):514-23. doi: 10.1016/0041-008x(90)90046-w.
Chronic inhalation of cigarette smoke in mice preferentially inhibited the antigen-specific T-cell proliferative response of lung-associated lymph nodes compared to anatomically distant lymph nodes. Cell mixing experiments demonstrated that the defect in smoked mice resulted from an abnormality in T-lymphocyte function. In contrast, the activity of antigen-presenting cells was similar in smoked and sham-smoked control animals. These results suggest that T-cell function in lung-associated lymphoid tissue may be inhibited in smokers, leading to a localized predisposition to respiratory tract infections.
与解剖位置较远的淋巴结相比，长期吸入香烟烟雾优先抑制了小鼠肺相关淋巴结的抗原特异性T细胞增殖反应。细胞混合实验表明，吸烟小鼠的缺陷是由T淋巴细胞功能异常所致。相比之下，吸烟小鼠和假吸烟对照动物体内抗原呈递细胞的活性相似。这些结果表明，吸烟者肺相关淋巴组织中的T细胞功能可能受到抑制，导致呼吸道感染的局部易感性。
