Myeloid C-type lectin receptor (MCLR)

Myeloid C-type lectin receptors (MCLRs) are a superfamily of pattern recognition receptors (PRRs) predominantly expressed on myeloid lineage cells, such as dendritic cells, macrophages, and neutrophils (Geijtenbeek & Gringhuis, Nat Rev Immunol 2009). These receptors are characterized by one or more C-type lectin domains (CTLDs) that facilitate the calcium-dependent recognition of specific carbohydrate moieties on the surface of pathogens, including fungi, bacteria, and viruses (Drouin et al., Front Immunol 2020). Beyond pathogen recognition, MCLRs are essential for sensing endogenous ligands released during tissue damage, thereby modulating inflammatory responses and maintaining homeostasis (Richardson & Williams, Front Immunol 2021). Signaling through MCLRs typically involves immunoreceptor tyrosine-based activation motifs (ITAMs) or hemITAMs, which recruit Syk kinase to trigger phagocytosis and the secretion of pro-inflammatory cytokines like IL-6 and IL-23 (Ostrop & Lang, Front Immunol 2017). In drug development, MCLRs are targeted to enhance the efficacy of vaccines through adjuvant activity or to reprogram the tumor microenvironment in oncology (Hoving et al., Front Immunol 2014). However, therapeutic manipulation of these receptors carries risks such as excessive cytokine release or the potential for inducing autoimmunity due to the broad role of MCLRs in immune regulation (Yan et al., J Transl Med 2015).

Other names

C-type lectin receptorCLRPattern recognition receptorC-type lectin-like receptorMyeloid CLR

Agonism of carbohydrate recognition domains to stimulate innate immune signaling and antigen cross-presentation, or antagonism to block pathogen entry and suppress pathological inflammation.