Anti-Mouse CD122 PE 50 ug
- Known as:
- Antibody toMouse CD122 PE 50 ug
- Catalog number:
- 12-1221-81
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD122 50
Related genes to: Anti-Mouse CD122 PE 50 ug
- 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
Related products to: Anti-Mouse CD122 PE 50 ug
Related articles to: Anti-Mouse CD122 PE 50 ug
- Although A2AR is a key immunoregulatory receptor that suppresses CD8 T cell activation in response to elevated extracellular adenosine in inflamed or hypoxic microenvironments, its role in CD8 T cell differentiation and cell-fate decisions during chronic viral infection and cancer remains poorly understood. Using A2AR-eGFP reporter mice, we show that A2AR expression is rapidly induced by TCR stimulation and persists under chronic antigen exposure and hypoxia, with sustained expression strongly associated with terminal exhaustion via the canonical Gα-cAMP-PKA pathway. Paradoxically, A2AR loss does not alleviate exhaustion but instead accelerates differentiation toward the terminally exhausted state. Single-cell multiomics profiling revealed that A2AR deficiency activates CD122 (IL-2Rβ)-dependent signaling, driving T cell exhaustion. Genetic deletion of CD122 in A2AR-deficient CD8 T cells reduced terminal exhaustion, identifying CD122 signaling as a key mediator of A2AR loss-driven exhaustion. Intriguingly, both sustained A2AR expression and A2AR loss converge to promote T cell exhaustion differentiation through distinct mechanisms. These findings uncover a paradoxical role of A2AR in shaping CD8 T cell fate choices during chronic infection and cancer. - Source: PubMed
Publication date: 2026/06/30
Song LongzhenKharel ArjunXie PingFan JieBaker AbuZhang YuqiZhang YiCui WeiguoZhang Bin - Palmoplantar pustulosis (PPP) carries substantial burden with limited treatments. Selective JAK1 inhibition is promising, yet prospective, immune-integrated data remain scarce. - Source: PubMed
Publication date: 2026/06/24
Xu ZhongruiChen WenyaoDu JingyuTian BiqingWang JiaqiMa SijieYang JiankangYu ChenCao TianyuLiu LingWang GangShao Shuai - Long-term survival of lung transplant recipients remains limited by chronic lung allograft dysfunction (CLAD). CLAD is only diagnosed following a persistent and substantial decline in lung function, after which irreversible damage to the lungs has occurred, limiting opportunities to effectively intervene at an early stage. There is a critical need for earlier detection prior to its clinical manifestation. The immunological drivers of CLAD remain unclear, limiting the development of predictive biomarkers and new therapies. - Source: PubMed
Publication date: 2026/06/23
Iacono GiuliaBegka ChristinaCardwell BaileyDaunt CarmelChatzis RoxannePattaroni CelineButler AlanaMacowan MatthewLevvey BronwynSnell Gregory IWestall Glen PMarsland Benjamin J - BPA exposure is known to be correlated with asthma incidence. This study aimed to investigate the molecular mechanisms underlying bisphenol A (BPA)-induced asthma. - Source: PubMed
Publication date: 2026/06/03
Gao GeHao YuqiuZhang LinLi WeiGao PengJia Yuxi - Sepsis, a life-threatening dysregulated host response to infection, involves complex cytokine signaling. Comprehensive bioinformatics analysis of cytokine activity, associated pathways, and immune alterations in sepsis is warranted. Using the sepsis dataset GSE26378 from GEO, we analyzed differential cytokine pathway activity with ssGSEA and identified differentially expressed genes (DEGs). Cytokine-related genes (CRGs) were extracted and overlapped with DEGs. Protein-Protein Interaction (PPI) network analysis and functional enrichment were performed on differentially expressed CRGs. Cytokine activity scores and pathway activities were quantified using Gene Set Variation Analysis (GSVA). Immune cell infiltration was assessed with MCP-counter. Machine learning algorithms (Random Forest, LASSO, SVM) identified diagnostic biomarkers, validated using an independent dataset (GSE26440) and ROC analysis. Cytokine/cytokine receptor pathways were significantly upregulated in sepsis. We identified 617 DEGs and 46 differentially expressed CRGs. Cytokine activity scores were significantly elevated in sepsis and strongly correlated with heightened activity in inflammatory pathways (e.g. TLR, IL-1R, NF-κB, JAK/STAT, hypoxia) and metabolic pathways (e.g. glycolysis, PI3K/AKT/mTOR). Immune analysis showed decreased T cells, NK cells, B cells, and cytotoxic lymphocytes, alongside increased neutrophils and endothelial cells; neutrophil infiltration positively correlated with cytokine scores. Machine learning identified four core genes (C3AR1, XCL1, CSF2RA, IL2RB), consistently dysregulated in sepsis across datasets and demonstrating robust diagnostic accuracy. This integrated bioinformatics study indicates heightened cytokine activity, profound alterations in inflammatory and metabolic pathways, and a dysregulated immune cell landscape in sepsis. The identified hub genes and the four-gene biomarker panel show potential as diagnostic tools, offering insights into sepsis pathophysiology. Insight box This study integrates multi-omics bioinformatics (ssGSEA, GSVA, PPI, immune deconvolution) and machine learning (RF, LASSO, SVM) to dissect sepsis pathophysiology. Innovatively, we quantify cytokine pathway hyperactivity, linking it to inflammatory/metabolic dysregulation (TLR, NF-κB, glycolysis) and immune imbalance. A novel four-gene panel (C3AR1, XCL1, CSF2RA, IL2RB) was identified and validated as a robust diagnostic biomarker, bridging cytokine signaling with clinical utility. The findings provide mechanistic insights into sepsis-driven immune-metabolic crosstalk and offer translational potential for early diagnosis and targeted therapy. - Source: PubMed
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