Sensing Tissue Damage by Myeloid C-Type Lectin Receptors
After both sterile and infectious insults, damage is inflicted on tissues leading to accidental or programmed cell death.
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).
Dectin-1 embraces Candida glabrata. No abstract available.
In this issue of Immunity, Warnatsch et al. (2017) describe how neutrophils measure their microbial opponents by differential shuttling of reactive oxygen species (ROS)
Candida albicans triggers a differential profile of microRNAs depending on its growing form. No abstract available.