Dexamethasone induced Dectin-1 activation enhances NLRP3 inflammasome activation.

ABSTRACT: Systemic candidiasis is a serious complication in immunocompromised patients, with Candida albicans emerging as the most common opportunistic pathogen. In various therapeutic treatment regimens the immunosuppressive agent Dexamethasone is used. Dexamethasone itself impairs the function of dendritic cells and reduces thereby their capacity for T-cell proliferation through the activation of Dectin-1 by β-glucans. In the present study, we reveal that these tolerogenic dendritic cells (Dex-DCs) have an increased secretion of IL-1ß and IL-18 when stimulated with β-glucans. We show an increased formation of ASC specks, which are crucial for recruiting pro-caspase-1, indicating an elevated inflammasomal activity. In line with this, we were able to show that treatment of tolerogenic dendritic cell

SUBMITTER: Koerber RM 

PROVIDER: S-EPMC12465279 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature