Anti_Human, mab CCR6 Source Mouse
- Known as:
- Anti_Human, mab CCR6 Source Mouse
- Catalog number:
- 101-M282
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Human mab CCR6 Source Mouse
Related genes to: Anti_Human, mab CCR6 Source Mouse
- Gene:
- CCR6 NIH gene
- Name:
- C-C motif chemokine receptor 6
- Previous symbol:
- STRL22
- Synonyms:
- CKR-L3, GPR-CY4, CMKBR6, GPR29, DRY-6, DCR2, BN-1, CD196
- Chromosome:
- 6q27
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-21
- Date modifiied:
- 2016-03-14
Related products to: Anti_Human, mab CCR6 Source Mouse
Related articles to: Anti_Human, mab CCR6 Source Mouse
- Inflammatory bowel disease (IBD) is a chronic, nonspecific inflammatory disorder affecting the gastrointestinal tract. The condition's pathology not only involves the digestive system but also can impact various organs and tissues throughout the body. Metabolic syndrome is a clinical syndrome characterized by obesity, insulin resistance, hypertension, and hyperlipidemia. Extensive research suggests a potential association between IBD and metabolic syndrome. - Source: PubMed
Publication date: 2026/04/14
Yin Yu-ZheYan Chao-ShengWu LingLi Guo-QingPei Xin-YuXue Yu-ZhengRen Yi-LinSun Hao-WenSheng Ying-Yue - Aging couples oxidative stress, inflammation, and leaky gut; ginsenosides are promising yet hobbled by poor conversion. We asked whether probiotic fermentation enriching PPD-type ginsenosides converts ginseng into a potent, low-dose antiaging agent. In D-galactose-aged mice, 20 mg/kg of probiotic-fermented ginseng (GFB) outperformed 600 mg/kg native ginseng: Rg3/Rg5/Rd and antioxidant capacity surged, cytokines fell, redox balance, barrier integrity, and youthful microbiota were restored. Plasma 20(S)-protopanaxadiol (PPD) increased 4-6-fold only in fermented-ginseng mice; PPD down-regulated barrier-destabilizing genes and docked stably into CC-chemokine receptor 6 (CCR6), suggesting a potential mechanism for blocking CCL20-driven chemotaxis. Thus, fermentation transforms ginseng into a food-grade, microbe-activated pro-drug that delivers systemic PPD, antagonizes CCR6, and simultaneously quells inflammation, seals the gut, and resets redox homeostasis for precision geroprotection. - Source: PubMed
Publication date: 2026/04/13
Huang XingdaLi JixiangNaveed MuhammadWang ZijieDu XuxuLi WutangWang YichengYuan DonglinWang ChaoranCheng QianChen ZhixianWu SijinHou BinbinLi MingLi Yuyuan - Immune checkpoint inhibitors (ICIs) universally enhance antitumor immunity but endanger a subgroup of patients by triggering immune-related adverse events (irAEs). We profiled the expressions of 41 proteins on peripheral blood mononuclear cells (PBMCs) prior the initiation of immunotherapy. CXCR3 and CCR6 expressions were significantly decreased in PBMC subpopulations from patient with irAEs but not from those who responded to PD-1 inhibitors. The expression of CCR6 in a NK cell subpopulation serves exclusively as a biomarker to differentiate patients who developed irAEs. Interestingly, circulating ligands of CXCR3, including CXCL9, CXCL10, and CXCL11, were significantly increased in patients who later developed irAEs after PD-1 inhibitor treatment. The decreases of CXCR3 in three T cell subpopulations and decreases of CCR6 in a NK cell subpopulation were further validated in two independent external cohorts. Moreover, multiple proteins in PBMCs, distinct from the irAE-predicting biomarkers, exhibited differential expression levels corresponding to the differential responses to the PD-1 inhibitors. Via multiple independent cohorts, our study revealed crucial roles of CXCR3 and CCR6 in PD-1-induced irAEs, provided potential circulating biomarkers associated with toxicity and responses of PD-1 inhibitors and further sculptured the landscape of immune cell heterogeneity via focusing on PBMC subpopulations. - Source: PubMed
Publication date: 2026/04/05
Wang JunXie HongGong YuanyuanLiu SonglinGuan YapingZhang YuekaiXie QiWang JingyiLi YeZeng XueqinChen XiWang Chen - Robust T helper 1 (Th1) cell responses, which activate macrophages to kill intracellular parasites, are required to control Leishmania infection. Yet, visceral leishmaniasis (VL) patients do not control the infection despite the expansion of CD4 T cells and increased IFN-γ expression in the spleen. Chemokines and/or chemokine receptors are involved in cellular migration and are critical in the inflammatory response. In a recent study that defined a transcriptional signature for CD4 T cells from active VL patients, we found several differentially expressed chemokine receptor genes in CD4 T cells compared to healthy endemic controls (EC). Since CD4 T cells play crucial roles in parasite clearance, a better understanding of the role of altered chemokine receptor expression on CD4 T cells and their different subsets during VL could inform future treatment strategies. In this study, we examined the gene expression and surface protein expression of differentially expressed chemokine receptors found in human VL subjects, relative to endemic controls (EC) by real-time qPCR and multicolor flow cytometry, respectively. We measured chemokine levels in plasma by enzyme-linked immunosorbent assay (ELISA) and performed transwell migration assays and flow cytometry to measure the migratory potential of CD4 T cell subsets. We found elevated mRNA and surface protein expression of CCR5, while reduced CCR4 and CCR6 expression in CD4 T cells from VL patients compared to EC. The frequency of CCR5 expressing Th1 cells was increased in peripheral blood, indicating the expansion of CCR5 Th1 cells that may be responsible for Th1 cells trafficking towards infected tissues. Lower CCR4 expression was found on regulatory T (Treg) cells and central memory T (Tcm) cells, possibly explaining the reduced frequencies of these cells in peripheral blood during VL. The frequency of CCR6 expressing CD4 T cells was also found to be lower in VL patients. Our results show that VL patients possess unique chemokine receptor expression patterns on the cell surface of CD4 T cells, compared to EC. We also found increased levels of CCL3, CCL5 and CCL20 in VL plasma compared to EC. However, no changes were observed for CCL17 levels in VL plasma compared to EC, but their levels increased following treatment. We also observed reduced migration of VL CD4 T cells, relative to other lymphocytes and mononuclear cells, irrespective of exogenous CCL5 presence. However, the frequency of CD4 T cells migrating in response to CCL5 in EC individuals was similar. Additionally, we noted the frequency of CCR5 Th1 cells was increased in VL patients compared to EC. However, no enhancement was seen in the migratory capacity of CCR5 CD4 T cells in the presence of recombinant CCL5. This suggests that the CCR5 receptor signalling pathway is less responsive towards exogenous CCL5, potentially due to high levels of CCL3 and CCL5 present in VL plasma, which may saturate surface CCR5. The upregulation of CCR5 expression and downregulation of CCR4 and CCR6 by CD4 T cells distinguished VL patients from healthy individuals. These findings provide new insights into VL pathogenesis and could direct the development of new and improved disease diagnostics and therapeutics for treatment of VL. - Source: PubMed
Upadhyay ShreyaKumar ShashiChauhan Shashi BhushanRoy RitirupaNeyaz AzizaSingh Siddharth SankarTiwari RahulNylen SusanneEngwerda ChristianSundar ShyamKumar Rajiv - Observational investigations have discerned a correlation between primary biliary cirrhosis (PBC) and rheumatoid arthritis (RA). The primary objective of this study is to elucidate the disease risk correlation between them in terms of genetics, and to explore the genes and signaling pathways involved. We acquired genome-wide association studies (GWAS) summary data for PBC and RA from distinct repositories: PBC data sourced from the IEU OpenGWAS database, and RA data obtained from the Finnish consortium. Employing a bidirectional two-sample Mendelian randomization (MR) approach, we scrutinized the disease risk correlation of PBC and RA. Subsequent to this analysis, we conducted a series of meticulous sensitivity assessments to gauge the robustness of our MR findings. These evaluations encompassed analyses for heterogeneity and horizontal pleiotropy, outlier identification, Leave-One-Out analysis, and assessments for adherence to normal distribution assumptions. Furthermore, we conducted an in-depth analysis of the genes and signaling pathways potentially involved in the disease risk correlation between PBC and RA. Finally, a difference analysis and receiver operating characteristic (ROC) curve analysis were conducted. The MR analysis conducted in this study revealed a significant positive disease risk correlation between PBC and RA (P < 0.001, odds ratio [OR] 95% confidence interval [CI] = 1.081 [1.036-1.128]). Moreover, reverse MR analysis also demonstrated a significant positive disease risk correlation between RA and PBC (P < 0.001, OR 95% CI = 1.702 [1.422-2.039]). Importantly, the bidirectional MR analysis detected no evidence of heterogeneity, horizontal pleiotropy, or outliers, and the results were not affected by single single nucleotide polymorphisms (SNPs). Additionally, the findings were consistent with a normal distribution. SNP-associated gene mapping was performed, identifying 14 candidate genes. Subsequent pathway enrichment analysis indicated that these genes were predominantly involved in the chemokine signaling pathway, JAK-STAT signaling pathway, and Th1/Th2 cell differentiation. Among them, IL12RB2, CCR6, and MANBA may serve as key mediators in the shared disease risk correlation architecture of PBC and RA. Further analysis of the differences identified a gene (MANBA). The ROC curve demonstrated the potential diagnostic value of MANBA. The findings of this study suggest a bidirectional disease risk correlation between PBC and RA, establishing them as mutually risk factors. In clinical practice, vigilance is paramount among patients diagnosed with RA regarding the potential development of PBC. Conversely, individuals presenting with PBC should undergo systematic screening for the presence of RA. The genes and pathways identified in this study as potentially contributing to the mutual disease risk correlation between PBC and RA provide valuable insights and lay the groundwork for future investigations into the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/04/06
Yang MingyiRen HonghaoRen XiaodongWen PengfeiXie JialeWan XianjieXu KeLiu LinHou WeikunYang ZhiXu Peng