Ask about this productRelated genes to: IL15Ra antibody
- Gene:
- IL15RA NIH gene
- Name:
- interleukin 15 receptor subunit alpha
- Previous symbol:
- -
- Synonyms:
- CD215, IL-15RA
- Chromosome:
- 10p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-08-10
- Date modifiied:
- 2016-04-25
Related products to: IL15Ra antibody
Related articles to: IL15Ra antibody
- Beyond conventional transcriptome profiling, RNA-sequencing (RNA-Seq) enables the discovery of variants within expressed genes linked to complex traits such as mastitis resistance or susceptibility. In this study, RNA-Seq was performed on milk somatic cells from uninfected Holstein cows with no history of mastitis (Neg, n = 9) or with subclinical intramammary infections (sIMI) caused by Prototheca spp. (P+ , n = 11) or Streptococcus agalactiae (Sa+ , n = 11). The objective was to identify transcriptome-derived sequence variants detectable under specific microbiological conditions that may contribute to the modulation of host transcriptional responses. By integrating these transcript-derived variants with quantitative trait locus (QTL) annotations and enrichment analyses, we aimed to highlight genomic regions functionally associated with mastitis susceptibility or resilience. - Source: PubMed
Publication date: 2026/05/17
Vanzin AliceBisutti VittoriaCánovas ÁngelaCecchinato AlessioGallo LuigiGiannuzzi DianaPegolo Sara - Interleukin-15 (IL-15) is expressed in various cancers, including melanoma, where it exists in distinct membrane-associated isoforms. Primary melanoma cells predominantly express the non-cleavable transmembrane form (tmbIL-15), while metastatic cells also express a cleavable membrane-bound form (mbIL-15) complexed with IL-15Rα. As tmbIL-15 is capable of reverse signaling upon IL-15Rα engagement, we investigated how this signaling axis modulates melanoma cell behavior across tumor stages. Transcriptomic analysis of melanoma patients revealed that high IL-15 expression correlates with immune activation, inflammation and epithelial-to-mesenchymal transition (EMT), along with coordinated upregulation of IL-15 receptor subunits. Proteomic profiling of melanoma cell lines stimulated with soluble IL-15Rα (sIL-15Rα) uncovered distinct, stage-specific responses. Although several proteins were commonly deregulated across cell lines, most showed opposite regulation in primary versus metastatic models, indicating that tmbIL-15 reverse signaling triggers context-dependent programs influenced by tumor progression. A stringent cross-comparison identified five proteins (PSAP, MARCKS, eEF1A1, DDX39B, and RACK1) as consistently and differentially regulated across tumor stages. Further comparison with published NK cell co-culture and EMT cytokine stimulation datasets revealed a subset of shared effectors, notably PSAP, TPM3 isoform 2 and MARCKS, suggesting that IL-15Rα-induced tmbIL-15 signaling is part of the immune editing phenomenon eliciting pro-tumoral activities complementary to the EMT process. Among these, PSAP emerged as the most robustly and consistently modulated effector, upregulated in primary melanoma cells and downregulated in metastatic ones upon sIL-15Rα stimulation. Its expression correlated positively with CD8+ T cell infiltration and negatively with NK cell infiltration, with distinct transcriptomic programs associated with high PSAP expression in primary versus metastatic settings. Altogether, these findings identify PSAP as a stage-specific mediator of tmbIL-15 reverse signaling in melanoma, integrating immune and EMT-related cues with potential implications for tumor progression and microenvironmental remodeling. - Source: PubMed
Publication date: 2026/04/15
Forcelloni SergioGiron-Michel JulienDel Boccio PieroCufaro Maria ConcettaDi Sebastiano AliceMariotti Francesca RomanaCiancaglini CeciliaChouaib SalemPadelli MaelVespa SimoneMac Giang DangEbert StefanBuart StéphanieMaggi EnricoMoretta LorenzoVacca PaolaTumino NicolaQuatrini LindaCaruana IgnazioAzzarone BrunoSantopolo Silvia - Wilms tumor (WT) is the most common pediatric kidney cancer. Tolerogenic dendritic cells (TolDCs) promote tumor immune evasion in the tumor microenvironment. Therefore, establishing a TolDC-based prognostic model for WT holds significant clinical value. We analyzed WT-related genes from The Cancer Genome Atlas and TolDC-associated datasets to identify shared differentially expressed genes using Venn analysis. Protein-protein interaction network analysis and machine learning algorithms (Boruta and Support Vector Machine Recursive Feature Elimination, SVM-RFE) were performed to screen candidate hub genes. A prognostic risk model was constructed using univariate Cox proportional hazards regression, with predictive performance evaluated by Kaplan-Meier survival analysis and receiver operating characteristic curves. Immune infiltration analysis, gene set enrichment analysis, and BioGRID were conducted to elucidate biological functions. Drug-gene interaction analysis was performed using the Drug Signature Database. A total of 181 co-expressed genes were identified. Among these, MSH2, CDH2, ALDH1A1, AURKA, CD274, FOSL2, IL15RA, GADD45B, TGM2, CXCR4, SOD2, and MT1E were selected as TolDC-associated biomarkers for WT. The prognostic model ultimately pinpointed ALDH1A1, CXCR4, and FOSL2 as key diagnostic biomarkers, supported by Kaplan-Meier survival analysis and ROC curves, which confirmed the model's robust predictive capacity for survival risk. Drug-gene interaction analysis predicted 335 potential therapeutic compounds targeting ALDH1A1, CXCR4, and FOSL2. Comprehensive bioinformatics analysis identified the prognostic biomarkers of WT related to TolDCs, providing new insights for personalized WT treatment. - Source: PubMed
Publication date: 2026/04/30
Sun XiaolanGao YaqingMeng KexinWang YixuanWang Bei - 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