Vimentin is an endogenous ligand for the pattern recognition receptor Dectin-1

Abstract

We conclude that vimentin is an endogenous, activating ligand for Dectin-1. Its presence in areas of artery wall inflammation and O₂⁻ production suggests that vimentin activates Dectin-1 and contributes to the oxidation of lipids and cholesterol accumulation in atherosclerosis.

Dectin-1 deficiency does not affect atherosclerosis development in mice

“…1DeE). These findings are in line with previous reports demonstrating dectin-1 on subsets of macrophages in human atherosclerotic lesions [5,7].…”

“…Using human monocytes the intermediate filament protein vimentin, which can be secreted upon activation [6], was recently identified as a potential endogenous ligand for dectin-1 inducing production of ROS [5]. We tested whether the same holds true for mouse macrophages.…”

“…Dectin-1 is a well-characterized receptor for b-glucans on macrophages and it plays a critical role in the host defense against fungi [4]. Recently, the intracellular filament protein vimentin was reported to function as an endogenous ligand for dectin-1 [5]. In vitro studies showed that binding of vimentin, which is released from macrophages upon inflammatory stimulation [6], can trigger the production of ROS [5] and this might further promote the atherogenic process.…”

“…In vitro studies showed that binding of vimentin, which is released from macrophages upon inflammatory stimulation [6], can trigger the production of ROS [5] and this might further promote the atherogenic process. The presence of vimentin in human atherosclerotic lesions in close proximity to dectin-1 positive macrophages was also demonstrated, suggesting a possible involvement of the vimentin-dectin-1 axis in the pathogenesis of atherosclerosis [5].…”

T-cell receptor–HLA-DRB1 associations suggest specific antigens in pulmonary sarcoidosis

“…As vimentin is a basic protein and can be secreted by activated macrophages, it may be abundant in inflammatory conditions [35]. Vimentin can bind to receptors (dectin 1) expressed on dendritic cells, macrophages and B cells, thereby loading and activating antigen-presenting cells [36]. Also, vimentin can be post-translationally modified and thereby become an auto-antigenic target, as shown in rheumatoid arthritis [37].…”