Macrophage Inducible C-Type Lectin (MINCLE)

CLEC4E; CLECSF9; C-Type Lectin Domain Family 4 Member E; C-Type(Calcium Dependent,Carbohydrate-Recognition Domain)Lectin,Superfamily Member 9

Macrophage Inducible C-Type Lectin (MINCLE)
MINCLE specifically interacted with Malassezia species, which cause the skin diseases tinea versicolor and atopic dermatitis, as well as fatal sepsis. Mutation analysis showed that Malassezia interacted with the mannose-binding motif of MINCLE. Glycoconjugate microarray analysis indicated that MINCLE bound alpha-mannose but not mannan, suggesting that the geometry of alpha-mannosyl residues on Malassezia species is recognized by MINCLE and distinguishes them from Candida, Aspergillus, and other fungal species. Malassezia-activated macrophages produced TNF and other inflammatory cytokines and chemokines. Macrophages from mice lacking Mincle showed impaired cytokine/chemokine production, and the mutant mice had diminished inflammatory responses.

Organism species: Homo sapiens (Human)

Organism species: Mus musculus (Mouse)

Organism species: Rattus norvegicus (Rat)