Williams D M, Grubbs B G, Kelly K, Pack E, Rank R G
Division of Infectious Diseases, Audie L. Murphy Memorial Veterans Hospital, San Antonio, Texas, USA.
Infect Immun. 1996 Sep;64(9):3916-9. doi: 10.1128/iai.64.9.3916-3919.1996.
The role of gamma-delta T cells in host resistance to Chlamydia trachomatis was characterized by using a murine model of pneumonia caused by the mouse pneumonitis agent (MoPn), murine C. trachomatis. At days 3 and 7 after infection, gamma-delta T-cell-deficient knockout mice had significantly higher levels of MoPn in the lungs than did immunologically intact controls. At day 20, paradoxically, gamma-delta T-cell-deficient mice were more resistant to MoPn than were controls. This increased resistance was not due to an increased production of toxic cytokines or interleukin-10 in controls on that day. Gamma-delta T cells play a role in protection early in MoPn infection, but they may be deleterious later in infection, as has been observed in models of salmonella and trypanosome infection.
利用由小鼠肺炎病原体（MoPn）引起的小鼠肺炎模型（鼠沙眼衣原体），对γδT细胞在宿主抵抗沙眼衣原体中的作用进行了表征。在感染后第3天和第7天，γδT细胞缺陷型敲除小鼠肺中的MoPn水平显著高于免疫健全的对照小鼠。矛盾的是，在第20天，γδT细胞缺陷型小鼠比对照小鼠对MoPn更具抵抗力。这种抵抗力的增加并非由于当天对照小鼠中有毒细胞因子或白细胞介素-10的产生增加所致。γδT细胞在MoPn感染早期发挥保护作用，但在感染后期可能有害，正如在沙门氏菌和锥虫感染模型中所观察到的那样。
