Rabbit Anti-Human CX3CR1, N-terminus
- Known as:
- Rabbit Antibody toHuman CX3CR1, N-terminus
- Catalog number:
- 129-10221
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rabbit Anti-Human CX3CR1 N-terminus
Related genes to: Rabbit Anti-Human CX3CR1, N-terminus
- Gene:
- CX3CR1 NIH gene
- Name:
- C-X3-C motif chemokine receptor 1
- Previous symbol:
- GPR13, CMKBRL1
- Synonyms:
- CMKDR1, V28, CCRL1
- Chromosome:
- 3p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-12
- Date modifiied:
- 2016-10-05
Related products to: Rabbit Anti-Human CX3CR1, N-terminus
Related articles to: Rabbit Anti-Human CX3CR1, N-terminus
- Hepatocellular carcinoma (HCC) is one of the leading causes of tumour-related death. T cells and cytokines play a critical role in tumour progression, but the T cell landscape correlated with HCC prognosis remains undepicted. - Source: PubMed
Cui GuangzuHu EryaPeng QingpingZhou XinZhao YuLiu HaicongWang XinwenChen YihongShen HongZeng ShanMa Jiayao - CD4 T cells specific for citrullinated (cit)-peptides are key players in RA immunopathogenesis. Characterising these cells and identifying features of healthy and RA-associated autoreactivity will provide valuable insight into disease mechanisms and form the basis of immune state biomarkers to facilitate the next generation of RA treatments. - Source: PubMed
Publication date: 2026/06/01
Stanway James APeters DanielWaller HelenLakey JeremyLemos Henrique De PaulaWilliams KristianDegnan AbbieDiboll JulieBaru Abdul MannanTough DavidPratt Arthur GHilkens Catharien M UAnderson Amy EIsaacs John D - Trained immunity involves the reprogramming of innate immune cells after an initial exposure, resulting in heightened inflammatory responses to subsequent stimuli and enhanced bactericidal capacity during infection. However, this pro-inflammatory state could also exacerbate chronic conditions like inflammatory bowel disease (IBD), which is characterized by persistent inflammation and microbial imbalance. It remains unclear how trained immunity influences IBD pathogenesis and whether it can be harnessed therapeutically. In our study, pretreatment with β-glucan reprogrammed bone marrow hematopoietic progenitors and peripheral monocytes, inducing a profound shift in monocyte plasticity and significantly reducing the severity of dextran sulfate sodium (DSS)-induced colitis. Adoptive transfer of bone marrow or peripheral monocytes from β-glucan-trained mice into naive mice conferred robust protection against colitis, demonstrating that this protective effect is transferable. Trained mice also displayed improved clearance of intestinal bacterial infections. Single-cell RNA sequencing revealed an expansion of reparative Cx3cr1 macrophages derived from Ly6C monocytes, correlating with accelerated colonic epithelial regeneration. Collectively, these findings reveal how β-glucan-induced trained immunity modulates monocyte differentiation to ameliorate experimental colitis, highlighting the potential of harnessing trained immunity as a therapeutic strategy to recalibrate innate immune responses and restore gut homeostasis in IBD, shedding light for future clinical applications. - Source: PubMed
Publication date: 2026/06/01
Lv YinyinFan YanyunGao QingxiangChen QiongyunHu YiqunWang LinShi HuaxiuChen ErmeiXu QinyuCai YingFan QingqiLi LinyingDu DanRen JianlinCheng Shih-ChinXu Hongzhi - The activation of microglia in the epileptic brain is a complex process. As a mediator of the inflammatory response of microglia, the role of High Mobility Group Box 2 (HMGB2) in epilepsy is not well understood. - Source: PubMed
Publication date: 2026/05/30
Li XinruWang YitingSheng DandanLiu JingYazgulyyeva BibiXiao BoZhou LuoLiu Weiping - Microglia are the resident macrophages of the brain and are central to neuroimmunology research. The roles of microglia are often probed by pharmacological depletion with CSF1R inhibitors or by genetic manipulation using Cre-lox systems, but microglia-specific genetic targeting remains challenging due to limited specificity or efficiency of Cre lines. We confirm that Cx3cr1 mice, widely used for microglial studies, also target multiple peripheral tissue macrophage populations that fail to turn over within the standard 4-week period intended to improve specificity. To overcome this limitation, we combined tamoxifen induction in Cx3cr1 mice with PLX5622 treatment to accelerate peripheral macrophage turnover. In a brain infection model, this strategy increased the specificity of gene deletion in microglia in Cx3cr1 mice and eliminated confounding contributions from peripheral macrophages. In sum, the use of a CSF1R inhibitor provides a solution to enhance the precision of microglial genetic manipulation using a common Cre line. - Source: PubMed
Publication date: 2026/05/29
Babcock Isaac WLabuzan Sydney AKelly Abigail GSchuster Anne EAlemu SebleworkSibley Lydia AMarchildon Anne EHarris Tajie H