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首页> 外文期刊>Infection and immunity >Genital tract infection with Chlamydia trachomatis fails to induce protective immunity in gamma interferon receptor-deficient mice despite a strong local immunoglobulin A response.
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Genital tract infection with Chlamydia trachomatis fails to induce protective immunity in gamma interferon receptor-deficient mice despite a strong local immunoglobulin A response.

机译：尽管有强烈的局部免疫球蛋白A反应，但沙眼衣原体的生殖道感染未能在γ干扰素受体缺陷型小鼠中诱导保护性免疫。

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CD4+ T cells have been found to play a critical role in immune protection against Chlamydia trachomatis infection. Since both humoral and cell-mediated antichlamydial immunity have been implicated in host protection, the crucial effector functions provided by the CD4+ T cells may rely on Th1 or Th2 functions or both. In the present study, we evaluated the development of natural immunity following vaginal infection with C. trachomatis serovar D in female gamma interferon receptor-deficient (IFN-gammaR-/-) mice with a disrupted Th1 effector system. We found that in comparison with wild-type mice, the IFN-gammaR-/- mice exhibited a severe ascending primary infection of prolonged duration which stimulated almost 10-fold-stronger specific local immunoglobulin A (IgA) and IgG responses in the genital tract. Following resolution of the primary infection and despite the augmented antibody responses to chlamydiae, the IFN-gammaR-/- mice were completely unprotected against reinfection, suggesting that local antibodies play a subordinate role in host protection against chlamydial infection. Immunohistochemical analysis of frozen sections of the genital tract revealed many CD4+ T cells in the IFN-gammaR-/- mice, with a dominance of interleukin 4-containing cells in mice following resolution of the secondary infection. However, in contrast to the findings with wild-type mice, the typical clusters of CD4+ T cells were not found in the IFN-gammaR-/- mice. Few and similarly distributed CD8+ T cells were observed in IFN-gammaR-/- and wild-type mice. Whereas chlamydia-infected macrophages from wild-type mice had no inclusion bodies (IB) and produced significant amounts of nitric oxide (NO) in the presence of IFN-gamma, macrophages from IFN-gammaR-/- mice contained many IB but no NO. These results indicate that CD4+ Th1 cells and IFN-gamma, rather than local antibodies, are critical elements in host immune protection stimulated by a natural ascending C. trachomatis infection in the female genital tract.
机译：已经发现CD4 + T细胞在针对沙眼衣原体感染的免疫保护中起关键作用。由于体液和细胞介导的抗衣原体免疫都与宿主保护有关，因此CD4 + T细胞提供的关键效应子功能可能依赖于Th1或Th2功能或两者。在本研究中，我们评估了在女性Thamma干扰素受体缺陷型（IFN-gammaR-/-）小鼠中，沙眼衣原体血清D感染阴道后，Th1效应器系统被破坏后自然免疫的发展。我们发现与野生型小鼠相比，IFN-gammaR-/-小鼠表现出持续时间延长的严重上升原发感染，刺激生殖道的特异性局部免疫球蛋白A（IgA）和IgG响应增强近10倍。在原发感染消退后，尽管抗体对衣原体的反应增强，但IFN-gammaR-/-小鼠完全不受再次感染的保护，这表明局部抗体在宿主对衣原体感染的保护中起次要作用。生殖道冰冻切片的免疫组织化学分析显示，IFN-gammaR-/-小鼠中有许多CD4 + T细胞，继发感染消退后，小鼠中的白介素4细胞占主导地位。但是，与野生型小鼠的发现相反，在IFN-gammaR-/-小鼠中未发现典型的CD4 + T细胞簇。在IFN-gammaR-/-和野生型小鼠中，观察到很少且分布相似的CD8 + T细胞。来自野生型小鼠的衣原体感染的巨噬细胞没有包涵体（IB），在IFN-γ存在下会产生大量的一氧化氮（NO），而来自IFN-gammaR-/-小鼠的巨噬细胞却含有许多IB，但没有NO 。这些结果表明，CD4 + Th1细胞和IFN-γ，而不是局部抗体，是女性生殖道中自然上升的沙眼衣原体感染所刺激的宿主免疫保护的关键要素。

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