Janet A. Willment

TL;DR: It is shown that Dectin-1 mediates the production of TNF-α in response to zymosan and live fungal pathogens, an activity that occurs at the cell surface and requires the cytoplasmic tail and immunoreceptor tyrosine activation motif of Dect in addition to Toll-like receptor (TLR)-2 and Myd88.

TL;DR: It is shown that deficiency of dectin-1, the myeloid receptor for β-glucan, rendered mice susceptible to infection with Candida albicans, and a signaling non–Toll-like pattern-recognition receptor required for the induction of protective immune responses is established.

TL;DR: Dectin-1 is defined as the leukocyte β-glucan receptor, first described over 50 years ago, and resolves the long-standing controversy regarding the identity of this important molecule, which is identified as a new target for examining the immunomodulatory properties of β- glucans for therapeutic drug design.

TL;DR: A family in which four women who were affected by either recurrent vulvovaginal candidiasis or onychomycosis had the early-stop-codon mutation Tyr238X in the beta-glucan receptor dectin-1, explaining why dectIn-1 deficiency was not associated with invasive fungal infections and highlighting the specific role of dect in human mucosal antifungal defense.

TL;DR: Using a novel mAb raised against dectin-1, it is shown that the receptor is not dendritic cell-restricted as first reported, but is broadly expressed, with highest surface expression on populations of myeloid cells (monocyte/macrophage and neutrophil lineages).