Interaction Between Dendritic Cells and Candida krusei β-Glucan Partially Depends on Dectin-1 and It Promotes High IL-10 Production by T Cells

Abstract

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.

β-Glucans from Trametes versicolor (L.) Lloyd Is Effective for Prevention of Influenza Virus Infection

“…Dectin-1 can trigger DCs to drive T cell responses against several different fungal pathogens, bacteria, viruses and tumors [19,20]. In this study, our data showed that β-glucans promote the expression of Dectin-1 in BMDCs, which may activate downstream signals to produce an immune response [21]. Mature DCs can express remarkable levels of the costimulatory molecules CD80/86, which promote T cell activation for immune function.…”

Dectin-1-Mediated Production of Pro-Inflammatory Cytokines Induced by Yeast β-Glucans in Bovine Monocytes

“…The expression of CLEC7A was decreased upon treatment with WGP-Dispersible and Zymosan, but not with WGP-Soluble (Supplementary Figure 7). Previous reports have shown a downregulation of Dectin-1 expression on the surface of human monocyte-and mouse bone marrow-derived dendritic cells and mouse bone marrow-derived macrophages in response to particulate b-glucan stimulation (39)(40)(41). However, no mention was made therein whether CLEC7A gene expression was also reduced.…”

β-glucan induced trained immunity enhances antibody levels in a vaccination model in mice

“…Previous reports showed that b-glucan adjuvanticity increases the expression of co-stimulatory molecules like CD86 and CD40 in dendritic cells via direct activation of Dectin-1, however, no training induced effects have been reported. 24,25 Therefore, we first tested if b-glucan training improved the expression of co-stimulatory molecules such as CD86 and CD40 on BMDMs in an in-vitro training model. In this experiment, 3 million BMDMs were trained with either PBS (untrained) or 100 µg/mL of b-glucan for 24 h in a 12-well plate with a total volume of 2 mL.…”