Toll‐like receptors (TLRs), TLR2 in particular, are shown to recognize various glycans and glycolipid ligands resulting in various immune effector functions. As barley β‐glucan and zymosan are the glycans implicated in immunomodulation, we examined whether these ligands interact with Dectin‐1, a lectin‐type receptor for glycans, and TLR2 and induce immune responses that can be used against Leishmania infection in a susceptible host. The binding affinity of barley β‐glucan and zymosan with Dectin‐1 and TLR2 was studied in silico. Barley β‐glucan‐ and zymosan‐induced dectin‐1 and TLR2 co‐localization was studied by confocal microscopy and co‐immunoprecipitation. These ligands‐induced signalling and effector functions were assessed by Western blot analyses and various immunological assays. Finally, the anti‐leishmanial potential of barley β‐glucan and zymosan was tested in Leishmania donovani ‐infected macrophages and in L. donovani‐infected BALB/c mice. Both barley β‐glucan and zymosan interacted with TLR2 and dectin‐1, but with a much stronger binding affinity for the latter, and therefore induced co‐localization of these two receptors on BALB/c‐derived macrophages. Both ligandsactivated MyD88‐ and Syk‐mediated downstream pathways for heightened inflammatory responses in L. donovani‐infected macrophages. These two ligands induced T cell–dependent host protection in L. donovani‐infected BALB/c mice. These results establish a novel modus operandi of β‐glucans through dectin‐1 and TLR2 and suggest an immuno‐modulatory potential against infectious diseases.

中文翻译：

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大麦β-葡聚糖和酵母聚糖在感染多巴氏利什曼原虫的BALB / c小鼠中诱导Dectin-1和Toll样受体2共定位和抗利什曼免疫反应。

尤其是Toll样受体（TLR），TLR2能够识别多种聚糖和糖脂配体，从而产生多种免疫效应子功能。由于大麦β-葡聚糖和酵母聚糖是涉及免疫调节的聚糖，因此我们检查了这些配体是否与聚糖的凝集素型受体Dectin-1和TLR2相互作用，并诱导可用于抵抗利什曼原虫的免疫反应。在易感宿主中感染。在计算机上研究了大麦β-葡聚糖和酵母聚糖与Dectin-1和TLR2的结合亲和力。通过共聚焦显微镜和免疫共沉淀研究了大麦β-葡聚糖和酵母聚糖诱导的dectin-1和TLR2的共定位。这些配体诱导的信号传导和效应子功能通过Western印迹分析和各种免疫学分析进行了评估。最后，在感染了利什曼原虫多诺万尼的巨噬细胞和多诺氏乳杆菌中测试了大麦β-葡聚糖和酵母聚糖的抗利什曼原虫潜能。感染的BALB / c小鼠。大麦β-葡聚糖和酵母聚糖均与TLR2和dectin-1相互作用，但对后者的结合亲和力更强，因此在BALB / c衍生的巨噬细胞上诱导了这两种受体的共定位。既ligandsactivated MyD88-和Syk介导的在提高的炎性反应的下游途径杜氏利什曼原虫的巨噬细胞感染的。这两个配体在感染多巴尼酵母的BALB / c小鼠中诱导了T细胞依赖性宿主保护。这些结果建立了通过dectin-1和TLR2的新型β-葡聚糖操作方式，并提出了针对传染病的免疫调节潜力。