C-Type Lectin Domain Family 4, Member E (CLEC4E) ELISA Kits

Human C-Type Lectin Domain Family 4, Member E (CLEC4E) interaction partners

1. Mincle has the ability to survey mycolate-derived glycolipids from actinomycetes, distinguishing non-pathogenic (e.g. Rhodococcus spp.) and pathogenic (e.g. Mycobacterium tuberculosis) species on the basis of alpha-chain length.

2. No association was detected with any of the SNPs analysed and susceptibility to tuberculosis.

3. combination adjuvant systems demonstrate markedly different immune activation with age, with combined DC activation via Macrophage-inducible C-type lectin and TLR7/8 representing a novel approach to enhance the efficacy of early-life vaccines.

4. 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

5. a nonredundant role for Clec4e in coordinating major biological pathways involved in atherosclerosis

6. CLEC4E expression is significantly upregulated in human masticatory mucosa during wound healing

7. The expression of Mincle increases significantly during the early period of Aspergillus fumigatus infection, while expression of eight corresponding cytokines changes. Mincle, as a pattern recognition receptor, may play a role in the early innate immune response of the corneal resistance against fungus.

8. Induction of Mincle by Helicobacter pylori and consequent anti-inflammatory signaling denote a bacterial survival strategy.

9. our findings identify mincle as a contributor to the inflammatory response after traumatic brain injury

10. results suggest that cholesterol crystals are an endogenous ligand for hMincle and that they activate innate immune responses

11. Data indicate that MINCLE receptor is able to mediate the response to trehalose-6,6-dimycolate (TDM) dependent on SYK kinase and CARD9 protein.

12. mincle is a fungal receptor that can suppress antifungal immunity and, as such, is a potential therapeutic target.

13. These results demonstrated that GroMM is a unique ligand for human Mincle that is not recognized by mouse Mincle.

14. Results show the molecular mechanism of glycolipid recognition through C-type lectin receptors, which may provide clues to rational design for effective adjuvants.

15. Macrophage-inducible C-type lectin is associated with anti-cyclic citrullinated peptide antibodies-positive rheumatoid arthritis in men.

16. Mincle is a potentially critical player in human B cell responses.

17. Data indicate an unusual pattern of reciprocal expression of Mincle on peripheral blood monocytes or neutrophils.

18. silencing of renal DNaseI gene expression initiates a cascade of inflammatory signals including activation of Toll like receptors and Clec4e, leading to progression of both murine and human lupus nephritis

19. Our data suggest that Mincle is induced in adipose tissue macrophages in obesity at least partly through the saturated fatty acid/TLR4/NF-kappaB pathway, thereby suggesting its pathophysiologic role in obesity-induced adipose tissue inflammation.

20. progenitor-derived mast cells expressed the macrophage-inducible C-type lectin receptor Mincle, and exposure of these cells to M. sympodialis induced up-regulation of the mRNA expression of Mincle

Mouse (Murine) C-Type Lectin Domain Family 4, Member E (CLEC4E) interaction partners

1. 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

2. Mincle activation by cholesterol sulfate causes the secretion of a range of proinflammatory mediators in response to skin damage.

3. this study shows that mincle inhibits neutrophils and macrophages apoptosis in Aspergillus fumigatus keratitis

4. Mincle is induced specifically on M1 macrophages, where Mincle-Syk signaling promotes and maintains inflammatory phenotypes of M1 macrophages in acute renal inflammation.

5. 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.

6. Mincle deletion results in TLR4-mediated inflammation.

7. Priming by Mincle-deficient dendritic cells (DCs).

8. Thus, macrophage activation by the corynebacterial cell wall relies on TLR2-driven robust Mincle expression and the cooperative action of both receptors.

9. 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

10. 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.

11. 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

12. this study shows a significant role for Mincle in Pneumocystis modulating host defense during infection

13. 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.

14. a nonredundant role for Clec4e in coordinating major biological pathways involved in atherosclerosis

15. 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

16. 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.

17. Mincle Activation and the Syk/Card9 Signaling Axis Are Central to the Development of Autoimmune Disease of the Eye

18. 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

19. The results indicate differential roles for Dectin-2 and Mincle in the generation of adaptive immune responses to F. pedrosoi fungal infection in mice.

20. 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.

Cow (Bovine) C-Type Lectin Domain Family 4, Member E (CLEC4E) interaction partners

1. Targeting the Mincle and TLR3 receptor using the dual agonist cationic adjuvant formulation 9 (CAF09) induces humoral and polyfunctional memory T cell responses in calves

2. The structure of an extended portion of the extracellular domain of mincle, beyond the minimal C-type carbohydrate recognition domain, also constrains the way the binding domains may interact on the surface of macrophages.

3. The data demonstrate how mincle bridges between the surfaces of the macrophage and the mycobacterium.

Guinea Pig C-Type Lectin Domain Family 4, Member E (CLEC4E) interaction partners

1. the function of the guinea pig homologue of Mincle (gpMincle) and MCL (gpMCL). gpMincle directly bound to trehalose-6,6'-dimycolate