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Gamma interferon levels during Chlamydia trachomatis pneumonia in mice.

机译:小鼠沙眼衣原体肺炎期间的γ干扰素水平。

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摘要

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 (nuu) and MoPn-resistant heterozygous (nu/+) mice. In vivo depletion of IFN-gamma in nuu mice led to exacerbation of infection. Fluorescence-activated cell sorter analysis disclosed induction of GL3 antibody-positive cells (putatively gamma/delta+ T cells) in nuu mouse lung during infection with MoPn. Treatment of nuu 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.
机译:研究了在鼠模型中针对鼠沙眼衣原体(小鼠肺炎药[MoPn])的宿主防御。 MoPn敏感的裸胸腺无胸腺(nu / nu)和抗MoPn的杂合子(nu / +)小鼠在肺部产生γ干扰素(IFN-γ)。 nu / nu小鼠体内IFN-γ的体内耗竭导致感染加剧。荧光激活细胞分选仪分析揭示了在MoPn感染过程中nu / nu小鼠肺中GL3抗体阳性细胞(可能是γ/δ+ T细胞)的诱导。用抗NK细胞抗体(抗亚细亚GM1抗体)或抗γ/δ细胞抗体(UC7-13D5)在体内治疗nu / nu小鼠不会显着降低肺中IFN-γ的产生。然而,用抗NK细胞的抗体治疗严重的联合免疫缺陷小鼠(缺乏γ/δ细胞)可显着降低肺IFN-γ水平。

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