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our results indicate that Mincle plays an important role in neutrophil infiltration and suggest that Mincle signaling may provide a therapeutic target for treating sepsis
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Mincle activation by cholesterol sulfate causes the secretion of a range of proinflammatory mediators in response to skin damage.
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this study shows that mincle inhibits neutrophils and macrophages apoptosis in Aspergillus fumigatus keratitis
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Mincle is induced specifically on M1 macrophages, where Mincle-Syk signaling promotes and maintains inflammatory phenotypes of M1 macrophages in acute renal inflammation.
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work implicates a novel innate immune driver of Con A hepatitis and, more broadly, suggests a potential role for Mincle in diseases governed by sterile inflammation.
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Mincle deletion results in TLR4-mediated inflammation.
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Priming by Mincle-deficient dendritic cells (DCs).
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Thus, macrophage activation by the corynebacterial cell wall relies on TLR2-driven robust Mincle expression and the cooperative action of both receptors.
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this study shows that immune activation in vitro and in vivo by trehalose esters of simple fatty acids requires two acyl chains of length and involves Mincle
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Attenuated neutrophil extracellular trap formation in Mincle-/- neutrophils correlates with impaired autophagy activation in vitro and in vivo, whereas reactive oxygen species formation in these neutrophils remained intact.
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We here show that Mincle gene expression was induced in alveolar macrophages and neutrophils in bronchoalveolar lavage fluids of mice and patients with pneumococcal pneumonia
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this study shows a significant role for Mincle in Pneumocystis modulating host defense during infection
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The authors report that microbial stimulation triggers Mincle (Clec4e) expression through the myeloid differentiation primary response gene 88 (MyD88) pathway; a process that does not require MCL (Clecsf8, Clec4d). Conversely, they show that MCL is constitutively expressed but retained intracellularly until Mincle is induced, whereupon the receptors form heterodimers which are translocated to the cell surface.
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a nonredundant role for Clec4e in coordinating major biological pathways involved in atherosclerosis
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this paper shows that mycobacterial cell envelope glycolipid TDM modulates TLR2-mediated IL-10 and IL-12p40 responses in macrophages through Mincle, which is, in turn, up-regulated by Mycobacterium bovis BCG
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Data show that Mincle, the inducible receptor for mycobacterial cord factor, is the key switch for the transition of macrophages from cytokine expression to high nitric oxide production.
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Mincle Activation and the Syk/Card9 Signaling Axis Are Central to the Development of Autoimmune Disease of the Eye
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work shows parallel networks of necroptosis-induced CXCL1 and Mincle signalling that promote macrophage-induced adaptive immune suppression and thereby enable pancreatic ductal adenocarcinoma progression
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The results indicate differential roles for Dectin-2 and Mincle in the generation of adaptive immune responses to F. pedrosoi fungal infection in mice.
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Mincle is essential for the activation of macrophages by trehalose glycolipids, the receptor does not play a role in the uptake of these glycolipids or of glycolipid-coated particles.
