The MI rats exhibited a higher arrhythmia score after programmed electric stimulation than that treated with Mincle siRNA, suggesting that the inhibition of Mincle attenuated foetal ventricular arrhythmias post-MI.
From our study findings, CLEC4Ers10841845 conferred protection against the development of pulmonary TB with a P value of <0.05 and odds ratio of <1 for all models of genetic inheritance.
MINCLE is a C-type lectin receptor that recognizes trehalose-6,6'-dimycolate or "cord factor," the most abundant glycolipid in Mycobacterium tuberculosis.
We synthesized and evaluated the immunostimulatory capacity of a library aryl trehalose derivatives and evaluated the structure activity relationship of the compounds in terms of the ability of compounds to engage the Mincle receptor, induce production of innate cytokines from human and murine cells, induce a pro-Th17 cytokine profile from primary human peripheral blood mononuclear cells and demonstrated efficacy in generating antibodies in combination with a tuberculosis antigen M72 in a mouse model.
Macrophage-inducible C-type lectin (Mincle) interacts with the γ-subunit of high-affinity IgE receptor (FcεRIγ) and activates Syk by recognizing its specific ligand, trehalose-6,6'-dimycolate, a glycolipid produced by Mycobacterium tuberculosis.
The C-type lectin receptor of family 4 member E (CLEC4E) confers protection against tuberculosis in laboratory animals but its function in influencing exposure or resistance to pulmonary tuberculosis (PTB) in humans remains obscure.
C-type lectin receptor 4e (Clec4e) recognizes the cord factor of Mycobacterium tuberculosis but also senses molecular patterns released by necrotic cells and drives inflammation.
Microglial macrophage-inducible C-type lectin (Mincle) receptor launches microglial innate immunity after SAH, and thereby achieves a key step of early cerebral injury in SAH.
Here, we show that cholesterol sulfate, a molecule present in relatively high concentrations in the epithelial layer of barrier tissues, is selectively recognized by Mincle (Clec4e), a C-type lectin receptor of the innate immune system that is strongly up-regulated in response to skin damage.
The MI rats exhibited a higher arrhythmia score after programmed electric stimulation than that treated with Mincle siRNA, suggesting that the inhibition of Mincle attenuated foetal ventricular arrhythmias post-MI.
In this study, we examined the potential role of macrophage-inducible C-type lectin (Mincle) for host defense against <i>Pneumocystis</i> Binding assays implementing soluble Mincle carbohydrate recognition domain fusion proteins demonstrated binding to intact <i>Pneumocystis carinii</i> as well as to organism homogenates, and they purified major surface glycoprotein/glycoprotein A derived from the organism.
Previous studies have reported the expression of Mincle in neuronal and glial cells of the brain, but its expression and role in pain processing at the spinal level remain to be determined.
Our aim was to explore the role of Macrophage-inducible C-type lectin (Mincle) within the PVN in augmenting sympathetic activity following MI,and whether NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome/IL-1β axis is involved in this activity.
Most Mincle immunoreactivity was localized within the grey matter and the dorsal and ventral horns of the lumbar spinal cord in naïve rats.A single intrathecal (i.t.) injection of trehalose-6,6-dibehenate (TDB), a Mincle ligand, induced mechanical allodynia.
The main focus of the present study is to describe the biological consequences of renal DNaseI shut-down and reduced chromatin fragmentation with a particular focus on whether exposed large chromatin fragments activate Toll like receptors and the necrosis-related Clec4e receptor in murine and human lupus nephritis.
In the early stage of acute kidney injury, M1 macrophages are proinflammatory and destructive.In this study, Lv et al. reveal that Mincle (macrophage-inducible C-type lectin, Clec4e) is expressed on M1 macrophages in acute kidney injury, and the kidney is protected in a murine model of cisplatin-induced renal injury by inhibiting Mincle expression on macrophages.
Mincle (macrophage-inducible C-type lectin, Clec4e) is a transmembrane pattern recognition receptor involving the innate immunity, but its role in kidney disease is still unexplored.
Animals and cells were randomly divided into control and A. fumigatus keratitis group, which were treated with Mincle ligand Trehalose-6,6-dibehenate (TDB), Mincle neutralizing antibody (MincleAb) or PBS before infection.