CD80
- Known as:
- CD80
- Catalog number:
- 11-287-C025
- Product Quantity:
- 0.025 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD80
Ask about this productRelated genes to: CD80
- Gene:
- CD80 NIH gene
- Name:
- CD80 molecule
- Previous symbol:
- CD28LG, CD28LG1
- Synonyms:
- B7.1, B7-1
- Chromosome:
- 3q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-14
- Date modifiied:
- 2016-10-05
Related products to: CD80
Activation B7-1 antigen,B7,B7,Cd80,Mouse,Mus musculus,T-lymphocyte activation antigen CD80Activation B7-1 antigen,B7,BB1,CD28LG,CD28LG1,CD80,CTLA-4 counter-receptor B7.1,Homo sapiens,Human,LAB7,T-lymphocyte activation antigen CD80Activation B7-1 antigen,CD80,Oryctolagus cuniculus,Rabbit,T-lymphocyte activation antigen CD80anti-CD80anti-CD80anti-CD80anti-CD80anti-CD80anti-CD80 (1G1)anti-CD80 (3D7)anti-CD80 (3E10)anti-CD80 (4A4)anti-CD80 (1G1)anti-CD80 (1G1) type: Primary antibodies host: Mouseanti-CD80 (2A2) Related articles to: CD80
- Pararamosis, or pararama-associated phalangeal periarthritis, is a neglected tropical disease affecting rubber tappers in the Amazon, caused by contact with the urticating bristles of the caterpillar. This condition leads to chronic synovitis and progressive cartilage degradation, key features shared with other osteoarticular conditions such as osteoarthritis. - Source: PubMed
Publication date: 2026/08/25
Pohl Paula CZapotoski Luiza N KSardinha Luiz RVillas-Boas Isadora MPidde GiselleTambourgi Denise V - Immune checkpoint inhibitor (ICI)-associated myocarditis is uncommon but has been described as an important and potentially fatal complication of cancer treatment. Increasing evidence from a variety of data sources have reframed this complication as part of ICI-associated myotoxicity (ICI-M), a systemic cardiomuscular syndrome in which myocarditis, myositis, conduction disease, ventricular arrhythmias, dysphagia, pseudo-myasthenic oculobulbar signs, and respiratory muscle failure may coexist. Elevated troponin with ICI use is not synonymous with myocarditis but instead should trigger a structured evaluation that considers symptoms, ECG findings, troponin and creatine kinase concentrations, structural and functional assessments including left ventricular function, pathology when feasible, and exclusion of alternative causes including other cardiotoxic therapies. The severity of ICI-M is heterogeneous and can now be stratified using the presence of active thymoma, cardiomuscular symptoms, low QRS-voltage, left ventricular ejection fraction <50%, and magnitude of troponin elevation. Low-risk cases such as patients with abnormal cardiac biomarkers only may be monitored closely, whereas severe ICI-M requires monitored admission, early respiratory and swallowing assessment, ICI interruption, and rapid multidisciplinary immunosuppression. Corticosteroids are generally recommended; however, severe, progressive, or refractory disease increasingly supports pathophysiology-directed-based therapies, including abatacept and ruxolitinib. Abatacept inhibits CD80/CD86-CD28 co-stimulation and can be titrated to CD86 receptor occupancy of the monocytes. Ruxolitinib inhibits Janus kinase/signal transducer and activator of transcription cytokine signaling pathway and may complement abatacept bioactivity. Evidence is promising for these therapies but not definitive, pending prospective trials. Rechallenge is often avoided but could be reassessed in selected patients under strict surveillance. - Source: PubMed
Publication date: 2026/08/31
Salem Joe-Elie - Eosinophils play an essential role in intestinal homeostasis, yet the mechanisms governing their functions in intestine remain poorly defined. β-Glucan, an immunomodulator, has been shown to alleviate colitis, but whether it acts through eosinophils and the underlying mechanisms remains unclear. Here we show that β-Glucan pretreatment significantly attenuated dextran sulfate sodium (DSS)‑induced colitis in wild-type mice but not in eosinophil-deficient mice, indicating an eosinophil-dependent protective effect. β‑Glucan increased the frequency and absolute number of colonic active eosinophils (A-Eos), which correlated with reduced disease severity. Mechanistically, β‑glucan upregulated interleukin-33 (IL‑33) expression in colon tissues. Colon conditioned medium (CM) from β‑glucan‑treated mice directly promoted the differentiation of bone marrow‑derived eosinophils (BM-Eos) into CD80⁺PD‑L1⁺ A‑Eos ex vivo, and this effect was completely reversed by IL-33 neutralization. Our findings identify a novel β-glucan-IL-33-A-Eos axis and provide a mechanistic basis for using β-glucan as an immunomodulatory strategy to prevent inflammatory bowel disease (IBD). - Source: PubMed
Publication date: 2026/09/07
Zhou JunLuo DanHu SujieZhu HaLi ZhiqingCui LikunYu ZhouCao XuetaoWang Chunmei - Synovial plasma cell infiltration predicts inadequate response to adalimumab in patients with rheumatoid arthritis (RA), yet the cellular and molecular mechanisms underlying this association remain unclear. This study aimed to dissect the functional heterogeneity of synovial plasma cells between adalimumab responders and non-responders at single-cell resolution, and to identify the molecular pathways driving treatment resistance. - Source: PubMed
Publication date: 2026/09/04
Li JianbinJiang HouhuiWu DengfengXiong ZhenfangPeng YilinZhao JunLiu PengchengWu Rui - Prolonged antibiotic use has led to increased bacterial resistance, making antibacterial peptides a promising alternative. We previously identified that the anti-apoptotic lncRNA-803 could encode short peptides, though their functions were unknown. - Source: PubMed
Publication date: 2026/08/20
Han ShuoJiang JunxiDuan WeiLuo LinDu NingWu WanxiongAn MingweiAilibieke GulaliyaAlgharib Samah AttiaLiu JunfengLuo Wanhe