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首页> 外文期刊>Infection and immunity >Nocardia farcinica Activates Human Dendritic Cells and Induces Secretion of Interleukin-23 (IL-23) Rather than IL-12p70
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Nocardia farcinica Activates Human Dendritic Cells and Induces Secretion of Interleukin-23 (IL-23) Rather than IL-12p70

机译：诺卡氏菌激活人树突状细胞并诱导白介素23（IL-23）而不是IL-12p70的分泌

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Studying the interaction of dendritic cells (DCs) with bacteria controlled by T-cell-mediated immune responses may reveal novel adjuvants for the induction of cellular immunity. Murine studies and the observation that nocardias infect predominantly immunosuppressed patients have suggested that these bacteria may possess an adjuvant potential. Moreover, adjuvants on the basis of the nocardial cell wall have been applied in clinical studies. Since the handling of adjuvants by DCs may determine the type of immune responses induced by a vaccine, the present study aimed at investigating the interaction of immature human monocyte-derived DCs with live or inactivated Nocardia farcinica in vitro and determining the cellular phenotypic changes as well as alterations in characteristic functions, such as phagocytosis, induction of T-cell proliferation, and cytokine secretion. Human DCs ingested N. farcinica and eradicated the bacterium intracellularly. DCs exposed to inactivated N. farcinica were activated, i.e., they developed a mature phenotype, downregulated their phagocytic capacity, and stimulated allogeneic T cells in mixed leukocyte reactions. Soluble factors were not involved in this process. To elucidate the potential adjuvant effect of N. farcinica on the induction of T-cell-mediated immune responses, we characterized the cytokines produced by nocardia-exposed DCs and detected substantial amounts of tumor necrosis factor alpha (TNF-α) and interleukin-12 p40 (IL-12p40). However, nocardia-treated DCs secreted only small amounts of IL-12p70, which were significantly smaller than the amounts of IL-23. Thus, N. farcinica activates DCs, but adjuvants based on this bacterium may have only a limited capacity to induce Th1 immune responses.
机译：研究树突状细胞（DCs）与受T细胞介导的免疫反应控制的细菌之间的相互作用可能揭示出新型佐剂，可诱导细胞免疫。小鼠的研究以及诺卡氏菌主要感染免疫抑制患者的观察表明，这些细菌可能具有佐剂潜力。此外，基于诺卡氏细胞壁的佐剂已被用于临床研究。由于DC处理佐剂可能决定疫苗诱导的免疫反应的类型，因此本研究旨在调查未成熟的人单核细胞衍生DC与活的或灭活的诺卡氏性诺卡氏菌在体外的相互作用，并确定细胞表型的变化。诸如吞噬作用，诱导T细胞增殖和细胞因子分泌等特征功能的改变。人类DC摄入法氏猪笼草，并在细胞内根除细菌。暴露于灭活的杆状芽胞杆菌的DC被激活，即它们发展出成熟的表型，下调吞噬能力并刺激混合白细胞反应中的同种异体T细胞。可溶性因素不参与此过程。为了阐明N. farcinica对诱导T细胞介导的免疫反应的潜在佐剂作用，我们对暴露于诺卡氏菌的DC产生的细胞因子进行了表征，并检测到大量的肿瘤坏死因子α（TNF-α）和白介素12 p40（IL-12p40）。但是，经诺卡氏剂处理的DC仅分泌少量的IL-12p70，而IL-12p70明显小于IL-23。因此，farcinica N. farcinica激活DC，但是基于这种细菌的佐剂可能仅具有有限的诱导Th1免疫应答的能力。

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