Clec10a, also known as C-type lectin domain family 10 member A, macrophage galactose-type lectin (MGL1), or CD301a, is a C-type lectin receptor that binds to carbohydrates with terminal N -acetylgalactosamine residues [2]. It is expressed in various cell types, such as immature DCs, monocyte-derived DCs, M2a macrophages, oocytes, and progenitor cells during embryonic development [2]. Clec10a is involved in initiating TH1, TH2, and TH17 immune responses, and inducing tolerance in naïve T cells, playing a crucial role in modulating innate and adaptive immunity [2].

NC/Nga mice carry a stop-gain mutation in Clec10a, and repair of this mutation using the CRISPR-Cas9 system ameliorated house dust mite (HDM)-induced dermatitis [1]. Similarly, Clec10a-/-mice on the C57BL/6J background showed exacerbated HDM-induced dermatitis [1]. Clec10a expressed on skin macrophages inhibits HDM-induced Toll-like receptor 4 (TLR4)-mediated inflammatory cytokine production through the inhibitory immunoreceptor tyrosine activating motif in its cytoplasmic portion [1].

In conclusion, Clec10a is a significant C-type lectin receptor involved in immune-related functions. Gene-knockout mouse models, such as Clec10a-/-mice, have revealed its role in regulating inflammation associated with HDM-induced dermatitis, suggesting its importance in skin homeostasis and potential as a target for treating allergic skin diseases [1].