Abstract
The macrophage-inducible C-type lectin (Mincle) is an innate immune receptor on myeloid cells sensing diverse entities including pathogens and damaged cells. Mincle was first described as a receptor for the mycobacterial cell wall glycolipid, trehalose-6,6′-dimycolate, or cord factor, and the mammalian necrotic cell-derived alarmin histone deacetylase complex unit Sin3-associated protein 130. Upon engagement by its ligands, Mincle induces secretion of innate cytokines and other immune mediators modulating inflammation and immunity. Since its discovery more than 25 years ago, the understanding of Mincle’s immune function has made significant advances in recent years. In addition to mediating immune responses to infectious agents, Mincle has been linked to promote tumor progression, autoimmunity, and sterile inflammation; however, further studies are required to completely unravel the complex role of Mincle in these distinct host responses. In this review, we discuss recent findings on Mincle’s biology with an emphasis on its diverse functions in immunity.
Highlights
Upon initial encounter with infectious invaders or cellular stress conditions, the host defense immune system has to rapidly recognize pathogens or danger signals as potentially harmful
TDM-mediated inhibition of IgG bead phagosome maturation required the inhibitory FcγRIIB, which suggests collaboration between macrophage-inducible C-type lectin (Mincle) and FcγRIIB receptor signaling pathways in modulating phagocytosis of IgG-opsonized TDM-containing particles (Figure 2) [85]. Corroborating this notion, association between Dectin-1 and FcγRIIB was previously shown to be required for the inhibition of neutrophil function by IgG1 immune complexes [86]
Great progress has been achieved to understand the role of Mincle in immunity
Summary
Upon initial encounter with infectious invaders or cellular stress conditions, the host defense immune system has to rapidly recognize pathogens or danger signals as potentially harmful For this purpose, innate immune cells, such as macrophages, dendritic cells (DCs), and neutrophils (PMN) use a limited number of pattern recognition receptors (PRRs), including toll-like receptors (TLRs), nucleotide-binding oligomerization domain-like receptors, and C-type lectin receptors (CLRs), which activate immediate anti-microbial effectors or other defense mechanisms. The list of pathogens recognized by Mincle has expanded tremendously, including Streptococcus (S.) pneumoniae, Fonsecaea (F.) monophora, Helicobacter (H.) pylori, L. major, Pneumocystis carinii as well as different Corynebacterium strains [19, 39,40,41,42,43]. Can the promiscuity of Mincle’s ligand interactions be explained by structural analogies between ligands?
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