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Interaction Between Dendritic Cells and Candida krusei β-Glucan Partially Depends on Dectin-1 and It Promotes High IL-10 Production by T Cells
Frontiers in Cellular and Infection Microbiology ( IF 4.6 ) Pub Date : 2020-11-27 , DOI: 10.3389/fcimb.2020.566661
Truc Thi Huong Dinh 1, 2 , Phawida Tummamunkong 2 , Panuwat Padungros 3 , Pranpariya Ponpakdee 3 , Lawan Boonprakong 4 , Wilasinee Saisorn 5 , Asada Leelahavanichkul 5 , Patipark Kueanjinda 6 , Patcharee Ritprajak 2, 7
Affiliation  

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.



中文翻译:


树突状细胞和克柔念珠菌 β-葡聚糖之间的相互作用部分依赖于 Dectin-1,它促进 T 细胞高产 IL-10



主持人-念珠菌属相互作用已被广泛研究白色念珠菌感染,重点逐渐转向非白色念珠菌物种。克柔梭菌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克柔梭菌至关重要。坎迪亚细胞壁β-葡聚糖在诱导宿主保护性免疫反应中发挥重要作用。然而,目前尚不清楚如何克柔梭菌β-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 的成熟和功能,以响应从细胞壁中分离出的 β-葡聚糖。白色念珠菌,热带念珠菌, 和克柔梭菌。这三个截然不同的念珠菌属β-葡聚糖对 DC 标记 CD11c 的表达和 DC 成熟具有不同的影响。此外,骨髓来源的 DC (BMDC) 显示出增强的细胞因子反应,其特征是在以下情况下大量产生白细胞介素 (IL)-10:克柔梭菌β-葡聚糖刺激。 BMDCs 刺激克柔梭菌β-葡聚糖增强了 T 细胞产生的 IL-10,同时增加了 BMDC 产生的 IL-10。 dectin-1 连接的抑制表明 DC 上的 dectin-1 与细胞壁 β-葡聚糖之间的相互作用根据念珠菌属物种。的影响C. 克鲁塞伊β-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克柔梭菌细胞壁成分。这些数据可能有助于开发治疗患有以下疾病的患者的新临床方法:克柔梭菌感染。

更新日期:2021-01-22
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