Mouse Anti-Human IL-15 Antibodies
- Known as:
- Mouse Antibody toHuman Interleukin-15 Antibodies
- Catalog number:
- RB-IP-01-115-500
- Product Quantity:
- 500
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Mouse Anti-Human IL-15 Antibodies
Related genes to: Mouse Anti-Human IL-15 Antibodies
- Gene:
- IL2RB NIH gene
- Name:
- interleukin 2 receptor subunit beta
- Previous symbol:
- IL15RB
- Synonyms:
- CD122
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-01-22
- Date modifiied:
- 2016-10-11
- Gene:
- IL15 NIH gene
- Name:
- interleukin 15
- Previous symbol:
- -
- Synonyms:
- IL-15, MGC9721
- Chromosome:
- 4q31.21
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-11
- Date modifiied:
- 2016-10-05
Related products to: Mouse Anti-Human IL-15 Antibodies
Related articles to: Mouse Anti-Human IL-15 Antibodies
- Major Depressive Disorder (MDD) is a serious mental illness, and neuroinflammation is increasingly recognized as a contributor to its pathogenesis; however, the underlying cellular and molecular mechanisms remain largely unknown. In this study, we performed single-nucleus RNA sequencing to profile prefrontal cortex transcriptomics in interleukin-15 receptor subunit alpha knockout (Il15ra) mice displaying depressive-like behaviors. Il15ra mice exhibited cell-type-specific transcriptomic alterations, particularly affecting synapse assembly. Co-expression network analysis identified two gene clusters predominantly linked to synaptic pathways in microglia, excitatory neurons, and interneurons, suggesting dysregulated neuron-microglial interactions in depression. Morphological analysis revealed microglial activation and synapse remodeling driven by enhanced neuron-microglia communication via the CX3CL1/CX3CR1 signaling pathway. Pharmacological inhibition of CX3CL1/CX3CR1 signaling using a CX3CR1 antagonist reversed depressive-like behaviors and microglia-mediated excessive synapse pruning caused by IL-15RA deficiency. Collectively, these findings demonstrate that IL-15RA deficiency contributes to depression onset by modulating microglia-mediated synaptic remodeling, highlighting a targetable neuroimmune pathway for therapeutic interventions in MDD. - Source: PubMed
Publication date: 2026/04/22
Tang YueHuang YuPan JingLi ChaolanYang JieTan XunminHu KanganWen LuXie PeijunLiu YuxiangXu HaotianCao ShixinZhang JianpingLi YifanLiu PingYuan MinghaoSong XiaodongWu JingHe YiWong Ma-LiLicinio JulioZheng Peng - Excessive macrophage activation is thought to be the primary cause of the cytokine storm that results in severe coronavirus disease 2019 (COVID-19) complications. The underlying mechanisms remain elusive, and more research is needed to find disease-critical genes and develop effective therapies. In this study, we used publicly accessible microarray datasets of cytokine storm in cultured human monocyte-derived macrophages challenged with cytokines, and employed bioinformatics, such as weighted gene co-expression network analysis (WGCNA) and differential expression analysis, to dissect gene expression profiles and identify putative disease-related molecules. Initially, three co-expression modules and related key genes were discovered, which highly correlated to macrophages challenged with cytokines. Then, a preliminary gene expression signature consisting of 203 upregulated and 24 downregulated genes was identified. Next, protein-protein interaction analysis and hub gene identification were used to identify 11 crucial hub genes, namely (), (), (), (), (), (), (), (), (), () and (). Then, the LINCS L1000 characteristic direction signatures search engine (L1000CDS2) was employed for drug repurposing studies. Dasatinib was predicted to be the leading therapeutic compound to perturb the gene signature of cytokine storm in human macrophages. Connectivity Map results suggested that dasatinib may normalize ICAM-1 expression. In addition, the results of molecular docking studies and molecular dynamics simulation revealed that dasatinib may spontaneously interact with ICAM-1 via several key residues and form a relatively stable protein-ligand complex. Overall, this work, based on an analysis of co-expression correlation networks, gene expression signatures and pivotal genes in human macrophages challenged with cytokines, combined with drug repurposing studies, demonstrated that dasatinib may interact with ICAM-1 and could be a potential candidate for cytokine storm. However, due to the limitations of computational approaches, further experimental validation is necessary. - Source: PubMed
Publication date: 2026/03/27
Chen ShaojunWu DapengZheng ZheLuo YiyuanZhang Lihua - Viral reservoir presents a significant challenge in HIV-1 cure. We previously observed that Thymosin α1 (Tα1) may restrict the reservoir through the IL-15 pathway. However, the precise mechanism remains to be fully elucidated. Peripheral blood mononuclear cells (PBMCs) were obtained from people living with HIV-1 (PLWH). In vitro, THP-1 cells were differentiated into mature monocyte-derived dendritic cells (MoDCs) and co-cultured with PBMCs under various conditions. Intracellular HIV-1 p24 levels, CD8+ T and NK cell functionality, and reservoir size were evaluated. In vitro, Tα1 stimulation of MoDCs resulted in significant immune response and secretion of IL-15/RA complex ( < 0.001). This interaction with IL-2 Rβ/γ receptors on T cells enhanced the intracellular secretion of CCL3/5, IFN-γ, and TNF-α in CD8+ T cells ( < 0.05), which inhibited p24 levels in CD4+ T cells ( = 0.002), and reduced HIV-1 integrated DNA levels ( = 0.012). Furthermore, the secretion levels of IFN-γ, TNF-α, and GZMB in NK cells and proportion of CD8+ T cells significantly increased following co-culture. These alterations were found to be markedly inversely associated with reservoir size and reactivation. However, these effects were observed in PBMCs from immunological responders (CD4+ T cell count > 350 cells/µL) rather than nonresponders. Tα1 enhances CD8+ T cell function, promotes T proliferation, and suppresses reservoir size and reactivation via IL-15 pathway activation in dendritic cells, which warrants testing in functional cure trials in the future. - Source: PubMed
Publication date: 2026/03/23
Chen ChaoyuXun JingnaWang JiangrongZhang RenfangQi TangkaiLiu LiZhang XinyuSong ZichenShen YinzhongLu HongzhouChen Jun - In this cross-sectional observational study, we investigated whether recreational exercise (RE) influences systemic inflammation in Hashimoto's thyroiditis (HT) across different disease severity groups. We analyzed 403 participants from the Croatian Biobank of Patients with HT (CRO-HT), including 173 controls and 230 HT patients (euthyroid, levothyroxine [LT4]-treated, and hypothyroid). Serum levels of 92 inflammatory proteins were measured using the Olink Target 96 Inflammation panel, and exercise status was assessed via structured questionnaires. Linear regression revealed distinct protein associations depending on thyroid status. In controls, RE was associated with reduced MMP-10 and FGF-5, reflecting cardiovascular and muscle benefits. In euthyroid patients, RE was associated with decreased CXCL9 and TRAIL, implicating reduced type 1 inflammation and vascular risk. LT4-treated patients showed increases in IL-15RA and IL-24 with RE, suggesting improved muscle metabolism and anti-inflammatory effects. In hypothyroid patients, RE was associated with reduced CCL20 and increased HGF, while changes in TRANCE and TWEAK indicated mixed effects on bone and immune regulation. Notably, RE was associated with reduced CXCL9 and CCL20, two proteins previously linked to HT risk. Overall, RE is associated with distinct changes in inflammatory profiles across HT disease severity groups, with the most favourable responses observed in LT4-treated patients, suggesting synergy with hormone therapy. - Source: PubMed
Publication date: 2025/10/25
Vuletić MarkoŽnidar VannaBarić Žižić AnaSladić SandaKaličanin DeanTorlak Lovrić VeselaCvek MajaPunda AnteBoraska Perica Vesna - Given the constraints inherent in current biomarkers and renal biopsy techniques for lupus nephritis (LN), this exploratory investigation was conducted to identify novel serum protein expression profiles through proximity extension immunoassay (PEA, Olink) in patients experiencing initial-onset LN for early identification of LN. - Source: PubMed
Publication date: 2025/11/04
Xiao DongmeiKong TongWang TinghuiHuang HuaQin WenZhao BaojingChen HaiboWu XiudiWang KaizheZheng Jianping