Dectin-1 Signaling Update: New Perspectives for Trained Immunity
The C-type lectin receptor Dectin-1 was originally described as the β-glucan receptor expressed in myeloid cells, with crucial functions in antifungal responses.
The C-type lectin receptor Dectin-1 was originally described as the β-glucan receptor expressed in myeloid cells, with crucial functions in antifungal responses.
Conventional type 1 dendritic cells (cDC1s) are central to antitumor immunity and their presence in the tumor microenvironment associates with improved outcomes in patients with cancer.
Myeloid cells are components of the innate immune system that represent the first line of defense.
After both sterile and infectious insults, damage is inflicted on tissues leading to accidental or programmed cell death.
Sensing tissue damage is an ancient function of immune cells that is central to the regulation of inflammation, tissue repair, and immunity.
Myeloid C-type lectin receptors (CLRs) comprise a family of receptors expressed by immune myeloid cells that share homologous C-type lectin domains.
Type-I conventional dendritic cells (cDC1s) are key in inducing adaptive immunity.
β-Glucan-induced trained immunity in myeloid cells leads to long-term protection against secondary infections.
Host injury triggers feedback mechanisms that limit tissue damage.
Myeloid C-type lectin receptors (CLRs) are important sensors of self and non-self that work in concert with other pattern recognition receptors (PRRs).