We previously reported that NK cells can promote type 1 T cell immune response that is essential for protection to a primary infection of Chlamydia muridarum. In this study, we have investigated the contribution of NK cells to memory T cells associated immunity during chlamydial infection. We have found that NK cell depletion led to impaired production of IFN-γ by memory T cells upon re-stimulation with chlamydial antigens in vitro. Mice with depleted NK cells also exhibited reduced type 1 T cell recall responses, with increased production of IL-4 from CD4⁺ T cells and a lower level of Chlamydia-specific IgG2a titers compared to control mice. In addition, Tregs response was significantly increased in mice with NK cell depletion. Moreover, NK cell-depleted mice showed an increased bacterial loads and more severe inflammatory pathological changes than control mice. These findings indicate that NK cells contribute to protective memory T cell associated immunity to chlamydial re-infection through modulating the cytokine pattern of T cell and inhibition of Tregs response.

我们先前曾报道NK细胞可以促进1型T细胞免疫反应，这对于保护原发性肝炎至关重要 鼠衣原体。在这项研究中，我们调查了衣原体感染期间NK细胞对记忆T细胞相关免疫的贡献。我们发现NK细胞耗竭导致衣原体抗原重新刺激后记忆T细胞的IFN-γ产生受损。体外。NK细胞耗竭的小鼠也表现出降低的1型T细胞召回反应，CD4 ⁺ T细胞的IL-4产量增加，而CD4 ⁺ T细胞的水平降低衣原体与对照小鼠相比，特异性IgG2a滴度更高。此外，NK细胞耗竭的小鼠中Tregs反应显着增加。此外，与对照小鼠相比，NK细胞耗竭的小鼠显示出增加的细菌负荷和更严重的炎症病理变化。这些发现表明，NK细胞通过调节T细胞的细胞因子模式和抑制Tregs应答，有助于保护性T细胞相关的免疫性衣原体再感染。