Host-Candida interaction has been broadly studied during Candida albicans infection, with a progressive shift in focus toward non-albicans Candida species. C. krusei is an emerging multidrug resistant pathogen causing rising morbidity and mortality worldwide. Therefore, understanding the interplay between the host immune system and C. krusei is critically important. Candia cell wall β-glucans play significant roles in the induction of host protective immune responses. However, it remains unclear how C. krusei β-glucan impacts dendritic cell (DC) responses. In this study, we investigated DC maturation and function in response to β-glucans isolated from the cell walls of C. albicans, C. tropicalis, and C. krusei. These three distinct Candida β-glucans had differential effects on expression of the DC marker, CD11c, and on DC maturation. Furthermore, bone-marrow derived DCs (BMDCs) showed enhanced cytokine responses characterized by substantial interleukin (IL)-10 production following C. krusei β-glucan stimulation. BMDCs stimulated with C. krusei β-glucan augmented IL-10 production by T cells in tandem with increased IL-10 production by BMDCs. Inhibition of dectin-1 ligation demonstrated that the interactions between dectin-1 on DCs and cell wall β-glucans varied depending on the Candida species. The effects of C. krusei β-glucan were partially dependent on dectin-1, and this dependence, in part, led to distinct DC responses. Our study provides new insights into immune regulation by C. krusei cell wall components. These data may be of use in the development of new clinical approaches for treatment of patients with C. krusei infection.

主持人-念珠菌交互作用已被广泛研究白色念珠菌感染，焦点逐渐转向非白色念珠菌物种。C. krusei是一种新兴的多重耐药病原体，导致全球发病率和死亡率上升。因此，了解宿主免疫系统和C. krusei至关重要。坎迪亚细胞壁β-葡聚糖在诱导宿主保护性免疫反应中起重要作用。但是，目前还不清楚如何C. kruseiβ-葡聚糖影响树突状细胞 (DC) 反应。在这项研究中，我们研究了 DC 成熟和响应从细胞壁分离的 β-葡聚糖的功能。白色念珠菌,C. 热带， 和C. krusei. 这三个不同的念珠菌β-葡聚糖对 DC 标志物 CD11c 的表达和 DC 成熟有不同的影响。此外，骨髓衍生的 DCs (BMDCs) 表现出增强的细胞因子反应，其特征是在随后产生大量的白细胞介素 (IL)-10C. kruseiβ-葡聚糖刺激。BMDCs 刺激C. kruseiβ-葡聚糖增加了 T 细胞产生的 IL-10，同时增加了 BMDCs 产生的 IL-10。dectin-1 连接的抑制表明 DCs 上的 dectin-1 与细胞壁 β-葡聚糖之间的相互作用因念珠菌物种。的影响C. kruseiβ-葡聚糖部分依赖于 dectin-1，这种依赖部分导致了不同的 DC 反应。我们的研究为免疫调节提供了新的见解C. krusei细胞壁成分。这些数据可能有助于开发新的临床治疗方法C. krusei感染。