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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >Dengue NS1 antigen contributes to disease severity by inducing interleukin (IL)-10 by monocytes
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Dengue NS1 antigen contributes to disease severity by inducing interleukin (IL)-10 by monocytes

机译：登革热NS1抗原通过单核细胞诱导白介素（IL）-10导致疾病严重程度

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摘要

Both dengue NS1 antigen and serum interleukin (IL)-10 levels have been shown to associate with severe clinical disease in acute dengue infection, and IL-10 has also been shown to suppress dengue-specific T cell responses. Therefore, we proceeded to investigate the mechanisms by which dengue NS1 contributes to disease pathogenesis and if it is associated with altered IL-10 production. Serum IL-10 and dengue NS1 antigen levels were assessed serially in 36 adult Sri Lankan individuals with acute dengue infection. We found that the serum IL-10 levels correlated positively with dengue NS1 antigen levels (Spearman's r=047, P<00001), and NS1 also correlated with annexin V expression by T cells in acute dengue (Spearman's r=063, P=0001). However, NS1 levels did not associate with the functionality of T cell responses or with expression of co-stimulatory molecules. Therefore, we further assessed the effect of dengue NS1 on monocytes and T cells by co-culturing primary monocytes and peripheral blood mononuclear cells (PBMC), with varying concentrations of NS1 for up to 96 h. Monocytes co-cultured with NS1 produced high levels of IL-10, with the highest levels seen at 24 h, and then declined gradually. Therefore, our data show that dengue NS1 appears to contribute to pathogenesis of dengue infection by inducing IL-10 production by monocytes.
机译：已显示登革热NS1抗原和血清白介素（IL）-10水平均与急性登革热感染中的严重临床疾病有关，并且还显示IL-10抑制了登革热特异性T细胞反应。因此，我们着手研究登革热NS1引起疾病发病机理以及与IL-10产生改变有关的机制。在36名患有急性登革热感染的成年斯里兰卡人中，连续评估了血清IL-10和登革热NS1抗原水平。我们发现血清IL-10水平与登革热NS1抗原水平呈正相关（Spearman's r = 047，P <00001），而NS1也与急性登革热中T细胞的膜联蛋白V表达呈正相关（Spearman's r = 063，P = 0001） ）。但是，NS1水平与T细胞反应的功能或共刺激分子的表达无关。因此，我们通过将原代单核细胞和外周血单核细胞（PBMC）与不同浓度的NS1共同培养长达96小时，进一步评估了登革热NS1对单核细胞和T细胞的影响。与NS1共培养的单核细胞产生高水平的IL-10，在24 h时达到最高水平，然后逐渐下降。因此，我们的数据显示登革热NS1似乎通过诱导单核细胞产生IL-10来促进登革热感染的发病机理。

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