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细胞生物学翻译

发布者:鑫达医学翻译 发布时间:2012-12-24阅读:

原文

The discrimination between protective and damaging immune responses during TB is extremely important for rational vaccine design. As BCG vaccination has  variable efficacy and lasts for a limited amount of time, revaccination with BCG or modified BCG strains, DNA vaccines or subunit vaccines are some potential strategies. We have recently shown that repetitive subcutaneous BCG vaccination in Mtb-infected mice results in an enhanced IL-17 response when compared to control mice. With the increase in IL-17 producing cells,  elevated expression of the proinflammatory cytokines TNF, IL-6, and MIP-2 also occurred oncurrently with an enhanced influx of neutrophils to the lungs. Importantly, this response is highly pathological causing extensive tissue damage without changing the protective immune response. The  enhanced accumulation of IL-17-producing cells in the lung is not a result of differentiation of these cells  in the dLN, but it is likely dependent on IL-23 expression locally and IL-23p19 deficient mice or IL-17 antibody blockade in this model, prevented neutrophil accumulation and the increased pathology. Interestingly, as the number of IFN-g producing cell was not affected by repetitive BCG vaccinations in the lungs, it appears that the IL-17 response became refractory to regulation by the IFN-g response. This is surprising, as IFN-g responses can  regulate IL-17 responses following BCG infection.

These data show that re-exposure of Mtb-infected mice to high antigen challenge, promotes further expansion of an ongoing Th17 response which causes extensive lung pathology associated with elevated recruitment of  neutrophils. Importantly, this enhanced Th17 response is supported locally by elevated expression of IL-23 and does not affect the protective immune response.

译文

TB期间防护性免疫应答与破坏性免疫应答对合理设计疫苗尤为重要。BCG接种具不同功效,且功效维持一定周期。接种BCG或修改BCG菌株、DNA疫苗或亚单位疫苗可能作为有效的治疗方案。 近期一项研究表明,与对照组相比,Mtb感染小鼠皮下重复接种BCG疫苗导致IL-17应答增强。 随着IL-17产生细胞数量增多,大量嗜中性粒细胞进入肺部,使得促炎性细胞因子(如TNF、IL-6及MIP-2)的表达发生上调。该应答可在不改变保护性免疫应答的情况下造成严重的组织病理损伤。肺部IL-17分泌细胞的积累并非源于淋巴结内IL-17分泌细胞的分化,但局部存在IL-23表达依赖。研究表明,IL-23p19缺陷小鼠或IL-17抗体阻断可避免嗜中性粒细胞积累,并增加病理性改变[74]。有趣的是,重复BCG接种不会影响肺部γ-干扰素分泌细胞的数量,这表明IL-17应答可能对γ-干扰素的调控并不敏感。奇怪的是,有研究表明BCG感染后γ-干扰素应答可调控IL-17的应答。

这些数据表明,Mtb感染小鼠重复接触高水平抗原激发时,可促进Th17应答的进一步扩散,进而导致大范围肺部病理学改变(与嗜中性粒细胞招募升高相关)。局部IL-23表达量升高可增强Th17应答,但不影响保护性免疫应答。
 


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