| http://purl.uniprot.org/citations/36078084 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/36078084 | http://www.w3.org/2000/01/rdf-schema#comment | "The C-type lectin receptors (CLRs) Dectin-1 and Dectin-2 are involved in several innate immune responses and are expressed mainly in dendritic cells, monocytes, and macrophages. Dectin-1 activation exacerbates obesity, inflammation, and insulin resistance/type 2 diabetes (T2D). However, the role of Dectin-2 is not clear in T2D. This study aims to evaluate the expression and function of Dectin-2 in peripheral blood mononuclear cells (PBMCs) isolated from diabetic patients and non-diabetic controls. Flow-cytometry and qRT-PCR were performed to evaluate the expression of Dectin-2 in different leukocyte subpopulations isolated from T2D patients (n = 10) and matched non-diabetic controls (n = 11). The functional activity of Dectin-2 was identified in PBMCs. CRP, IL-1β, and TNF-α concentrations were determined by ELISA. siRNA transfection and Western blotting were performed to assess p-Syk and p-NF-kB expression. siRNA transfection was performed to knock down the gene of interest. Our results show that Dectin-2 expression was the highest in monocytes compared with other leukocyte subpopulations. The expression of Dectin-2 was significantly increased in the monocytes of T2D patients compared with non-diabetic controls. Dectin-2 expression positively correlated with markers of glucose homeostasis, including HOMA-IR and HbA1c. The expression of inflammatory markers was elevated in the PBMCs of T2D patients. Interestingly, SOCS3, a negative regulator of inflammation, was expressed significantly lowlier in the PBMCs of T2D patients. Moreover, SOCS3 expression was negatively correlated with Dectin-2 expression level. The further analysis of inflammatory signaling pathways showed a persistent activation of the Dectin-2-Syk-NFkB pathway that was instigated by the diminished expression of SOCS3. Dectin-2 activation failed to induce SOCS3 expression and suppress subsequent inflammatory responses in the PBMCs of diabetic patients. siRNA-mediated knockdown of SOCS3 in PBMCs displayed a similar inflammatory phenotype to diabetic PBMCs when exposed to Dectin-2 ligands. Altogether, our findings suggest that elevated Dectin-2 and its relationship with SOCS3 could be involved in the abnormal immune response observed in T2D patients."xsd:string |
| http://purl.uniprot.org/citations/36078084 | http://purl.org/dc/terms/identifier | "doi:10.3390/cells11172670"xsd:string |
| http://purl.uniprot.org/citations/36078084 | http://purl.uniprot.org/core/author | "Ahmad R."xsd:string |
| http://purl.uniprot.org/citations/36078084 | http://purl.uniprot.org/core/author | "Al-Mulla F."xsd:string |
| http://purl.uniprot.org/citations/36078084 | http://purl.uniprot.org/core/author | "Al-Rashed F."xsd:string |
| http://purl.uniprot.org/citations/36078084 | http://purl.uniprot.org/core/author | "Albaqsumi Z."xsd:string |
| http://purl.uniprot.org/citations/36078084 | http://purl.uniprot.org/core/author | "Haider M.J.A."xsd:string |
| http://purl.uniprot.org/citations/36078084 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
| http://purl.uniprot.org/citations/36078084 | http://purl.uniprot.org/core/name | "Cells"xsd:string |
| http://purl.uniprot.org/citations/36078084 | http://purl.uniprot.org/core/pages | "2670"xsd:string |
| http://purl.uniprot.org/citations/36078084 | http://purl.uniprot.org/core/title | "SOCS3 Regulates Dectin-2-Induced Inflammation in PBMCs of Diabetic Patients."xsd:string |
| http://purl.uniprot.org/citations/36078084 | http://purl.uniprot.org/core/volume | "11"xsd:string |
| http://purl.uniprot.org/citations/36078084 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/36078084 |
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