Williams D M, Grubbs B G, Schachter J, Magee D M
Division of Infectious Diseases, The Audie L. Murphy Veteran's Administration Hospital, San Antonio, Texas.
Infect Immun. 1993 Aug;61(8):3556-8. doi: 10.1128/iai.61.8.3556-3558.1993.
Host defense against murine Chlamydia trachomatis (mouse pneumonitis agent [MoPn]) in a murine model was investigated. Gamma interferon (IFN-gamma) was produced in the lungs by both MoPn-susceptible nude athymic (nu/nu) and MoPn-resistant heterozygous (nu/+) mice. In vivo depletion of IFN-gamma in nu/nu mice led to exacerbation of infection. Fluorescence-activated cell sorter analysis disclosed induction of GL3 antibody-positive cells (putatively gamma/delta+ T cells) in nu/nu mouse lung during infection with MoPn. Treatment of nu/nu mice in vivo with antibody to NK cells (anti-asialo GM1 antibody) or to gamma/delta cells (UC7-13D5) did not significantly decrease IFN-gamma production in the lung. However, treatment of severe combined immunodeficiency mice (which lack gamma/delta cells) with antibody to NK cells significantly reduced lung IFN-gamma levels.
研究了小鼠模型中宿主对鼠沙眼衣原体（小鼠肺炎病原体[MoPn]）的防御机制。易感染MoPn的裸无胸腺（nu/nu）小鼠和抗MoPn的杂合（nu/+）小鼠的肺部均产生了γ干扰素（IFN-γ）。在nu/nu小鼠体内消耗IFN-γ会导致感染加剧。荧光激活细胞分选分析显示，在感染MoPn期间，nu/nu小鼠肺中诱导了GL3抗体阳性细胞（推测为γ/δ+T细胞）。用抗NK细胞抗体（抗去唾液酸GM1抗体）或抗γ/δ细胞抗体（UC7-13D5）对nu/nu小鼠进行体内治疗，并未显著降低肺中IFN-γ的产生。然而，用抗NK细胞抗体治疗严重联合免疫缺陷小鼠（缺乏γ/δ细胞）可显著降低肺中IFN-γ水平。
