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.
MINCLE is a C-type lectin receptor that recognizes trehalose-6,6'-dimycolate or "cord factor," the most abundant glycolipid in 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.
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.
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.
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.
Lastly, corneal epithelium of 54 patients with Aspergillus fumigatus keratitis and 13 ocular trauma patients were collected to detect expression of Mincle by real-time RT-PCR, and 12 FK and 10 ocular trauma paraffin samples were collected to confirm expression of Mincle by immunohistochemistry.
Higher levels of Mincle mRNA and protein, as well as epithelial thickness and presence of inflammatory cells in the stroma, were observed in the AF group compared to control.
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.
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.
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.
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.
Macrophage-inducible C-type lectin (Mincle), a pattern recognition receptor, is a critical component of the innate immune system that is involved in the pathogenesis of chronic pain.
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.
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.