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发表时间:2019-2-11  浏览次数:243  
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原文:
As discussed, TGF-b is a central cytokine in the differentiation of Th17 cells; however this cytokine also acts in the differentiation of Foxp3-expressing Treg cells. It has  been shown that foxp3- expressing Treg cells expand during experimental Mtb infection and upon deletion Mtb bacterial burdens decrease. In humans, there are  more treg cells in active TB patients than patients with latent infection or in healthy tuberculin responders. Overall these data suggest a largely negative role for Treg cells in TB; however their presence in the infected organs may be important for balancing protective and damaging immune responses.
As both Th17 and Treg cells are present during Mtb infection it is important to understand what regulates the relative levels of each population.  TGF-b induces expression of foxp3 but further signaling by STAT-3-activating cytokines such as IL-6 promotes Th17 differentiation. As Mtb  induces early secretion of both IL-6 and IL-23, Th17 development is promoted, while Treg cells expand from a population of preexisting foxp3-expressing cells. It is  still  not clear what factors promote expansion of Treg cells during TB; however, the relative levels of RORgt and foxp3 expression as determined by the amount of TGF-b and STAT-3 signaling cytokines will certainly be important for the relative levels of Th17 and Treg cells. Therefore, during inflammatory responses where IL-23 and IL-6 are highly expressed, Treg cells may not expand efficiently and inflammation may develop without regulation. Further research is required to clarify this subject. In addition, recent data suggest an increased plasticity in Treg cells and Th17 cell; indeed, Treg cells can be converted into IL-17 producers by pathogen components or inflammatory mediators, such as IL-6. Treg conversion into IL-17 producers is yet to be analyzed in TB, but it may be of paramount importance in the regulation of inflammation and control of bacillary growth, as it is possible that sustained expression of IL-6 and IL-23 in the lungs of infected animals promote conversion of Treg cells into IL-17 producers.

译文:

TGF-β在Th17细胞分化方面具有重要作用。但该因子还在表达Foxp3的Treg细胞分化方面具有重要作用。另外一项研究表明,Mtb感染动物模型表达foxp3的Treg细胞含量增加。敲除foxp3后,载菌量降低。人类研究表明,活动性TB患者体内Treg细胞含量较潜伏期患者明显增多。此外,其Treg细胞含量较健康结核菌素应答者也较多。这些数据表明,Treg细胞在TB发病中具有负调控作用。但感染器官内Treg细胞的存在可能在维持保护性应答及损伤性免疫应答间平衡方面具一定作用。

Mtb感染期间感染部位检测到Th17与Treg细胞存在,可借此研究各细胞群体的调控情况。TGF-β可诱导foxp3表达,而STAT-3激活细胞因子(如IL-6)可促进Th17细胞分化[24,25,84]。Mtb感染后,早期IL-6与IL-23分泌量增加,促进Th17发育。同时,foxp3表达细胞类群形成Treg细胞。TB发病期间Treg细胞扩散的机制尚不清楚,但研究证实RORγt与foxp3表达在Th17细胞及Treg细胞含量方面具重要作用。

因此,炎症应答期间(IL-23与IL-6高表达),如Treg细胞未得到显著扩散,炎症将得以加重。需要进一步研究加以证实。近期研究表明,Treg细胞及Th17细胞具较高的可塑性。Treg细胞可借助病原体结构或炎症调节因子(如IL-6)产生IL-17[89]。TB发病后,Treg细胞是否能产生IL-17还需要进一步验证。但Treg细胞在炎症调节及细菌增殖抑制方面具有重要作用。我们推测感染动物肺部IL-6及IL-23维持表达可促成Treg细胞产生IL-7。

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