Anti-Human CD8a PE 25 ug
- Known as:
- Antibody toHuman CD8a PE 25 ug
- Catalog number:
- 12-0088-80
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD8a 25
Related genes to: Anti-Human CD8a PE 25 ug
- Gene:
- CD8A NIH gene
- Name:
- CD8a molecule
- Previous symbol:
- CD8
- Synonyms:
- -
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: Anti-Human CD8a PE 25 ug
Related articles to: Anti-Human CD8a PE 25 ug
- The risk profile of valvular heart disease (VHD) and its underlying mechanisms remain poorly understood. This study aimed to develop and validate a multi-omics-based risk prediction model, and to elucidate potential biological mechanisms. Using data from the UK Biobank, Cox proportional hazards and machine learning models (XGBoost and LightGBM) were evaluated for predicting VHD and its subtypes (aortic valve stenosis, AVS; aortic valve regurgitation, AVR; mitral valve regurgitation, MVR). Cox models based on key clinical factors showed the best predictive performance (C-index of 0.75-0.81), which was further enhanced by incorporating proteomic data (all C-index > 0.81) but not by genomic or metabolomic data. Notably, a simplified 10-year model comprising only four top proteins maintained favorable performance (C-index of 0.75-0.82). Cluster analysis identified blood pressure and lipid levels as leading modifiable risk factors for VHD onset. Functional enrichment analysis revealed that VHD is primarily associated with protease inhibition, AVS with fibrotic and matrix metabolic pathways, and MVR with immune-inflammatory activation. Mendelian randomization and Bayesian colocalization analyses suggested causal associations between CNTN5 and CD8A with risks of AVS and MVR, whilst IGFBP7 showed a reverse-direction association with AVS. These findings highlight promising avenues for early diagnostic biomarkers and potential precision-targeted therapies. - Source: PubMed
Publication date: 2026/07/06
Jiang ZhihaoLiu YangSong MingyuChen NingYu CanqingLv JunWan Eric Yuk FaiQi LuLi LimingSun DianjianyiZheng Bang - Guillain-Barré syndrome (GBS) is an acute immune-mediated neuropathy triggered by infections, with poorly understood pathophysiological diversity. COVID-19-associated GBS (COVID-GBS) is a rare but severe post-infectious condition, and its immune mechanisms remain unclear. We profiled immune mediators in cerebrospinal fluid (CSF) and serum from COVID-GBS patients, comparing them to non-COVID GBS (Control-GBS), COVID-19 patients without neurological complications (COVID-no-GBS) and non-inflammatory neuropathy controls (Neuropathy-no-GBS). To gain mechanistic insights, we integrated publicly available single-nucleus transcriptomic data from sural nerve biopsies of neuropathy patients. IL-8 was confirmed as a key cytokine in GBS. Analysis of publicly available single-nucleus transcriptomic data from non-GBS sural nerve biopsies suggested myeloid cells as potential sources of IL-8, with evidence of autocrine signaling capacity. LIF and CD8A emerged as novel biomarkers, with this transcriptomic analysis indicating that LIF receptor components are expressed on endothelial and stromal cells, suggesting these as potential cellular targets. COVID-GBS patients exhibited unique CSF alterations and distinct serum profiles marked by altered NK cell activity, cytotoxic T-cell responses, and myeloid differentiation. Moreover, associations between inflammatory, extracellular matrix, and regulatory markers with clinical disability differed between COVID-GBS and Control-GBS, pointing to divergent immune mechanisms. Our findings suggest that GBS involves myeloid-driven cytokine responses and local LIF signaling. Analysis of publicly available transcriptomic data from non-GBS sural nerve biopsies suggests potential cellular sources and targets, though validation in GBS-affected tissue is needed. COVID-GBS features a distinct immune signature involving localized and systemic inflammation. These insights deepen our understanding of GBS pathogenesis and nominate candidate biomarkers for further validation and potential therapeutic targeting. - Source: PubMed
Publication date: 2026/07/04
Ulutekin CanCan AmelieSúkeníková LenkaQuerol LuisJuntas-Morales RaulLlauradó ArnauDietmann AneliaWeiss TobiasLatorre DanielaBecher BurkhardIngelfinger FlorianSchreiner Bettina - Chronic hepatitis B virus (HBV) infection is a major etiological driver of hepatocellular carcinoma (HCC) and is accompanied by profound immune dysregulation that shapes disease progression and therapeutic responsiveness. However, the extent to which systemic immunity reflects the tumor immune microenvironment (TIME) in HBV-related HCC (HBV-HCC) remains incompletely defined. Here, we used mass cytometry (CyTOF) to resolve immune heterogeneity across peripheral blood mononuclear cells (PBMCs), tumor tissues, and matched adjacent non-tumor (paracancer) tissues in treatment-naïve HBV-HCC. PBMCs, tumor tissues, and paracancer tissues were collected from 12 treatment-naïve HBV-HCC patients and profiled by CyTOF. Nine major immune lineages/clusters were quantified and compared across compartments. Immune-cell distributions were correlated with virological and clinicopathological features (HBV DNA status, serum alpha-fetoprotein [AFP], tumor differentiation) and 5-year clinical outcomes. Public transcriptomic datasets were further leveraged for external validation of CD8A/CD8B-associated prognostic signals. HBV-HCC exhibited marked systemic-local immune compartmentalization. PBMCs were enriched for naïve CD8⁺ T cells and natural killer (NK) cells, whereas paracancerous tissues showed higher abundance of myeloid-derived suppressor cells (MDSCs) and memory CD8⁺ T cells. In contrast, HCC tissues were characterized by increased neutrophils and regulatory T (Treg) cells, together with a more activated and immunosuppressive marker profile in HCC-associated MDSCs. HBV DNA-positive patients showed higher intratumoral expression of naïve CD8⁺ T cells and Tregs than HBV DNA-negative patients, with the increase being most evident in HCC tissues relative to matched paracancerous tissues. Clinically aggressive phenotypes, including high AFP, poor differentiation, and postoperative recurrence, were characterized by neutrophil expansion accompanied by reduced PD-1⁺ dendritic cells (PD-1⁺ DCs) and decreased naïve/memory CD8⁺ T-cell subsets. Although higher CD8A/CD8B expression in public datasets predicted improved survival, CyTOF indicated that abundant intratumoral CD8⁺ infiltration could coexist with systemic and intratumoral immunosuppression and functional exhaustion, consistent with the recognized challenge of reinvigorating exhausted intrahepatic immunity. HBV-HCC is defined by profound immune heterogeneity across blood, tumor, and adjacent non-tumor compartments. Distinct immune signatures associate with virological activity, tumor aggressiveness, and long-term outcomes, providing a rationale for immune-based patient stratification and for combinatorial immunotherapy strategies targeting both myeloid-driven suppression and dysfunctional T-cell immunity. - Source: PubMed
Publication date: 2026/07/02
Li YadiWang WenjingZeng AjuanZheng XiaoqinLyu LingnaDing HuiguoWang Shanshan - Tumor-associated macrophages (TAMs) are a major immune component of the glioblastoma microenvironment, but macrophage-oriented transcriptomic stratification remains difficult to reproduce across datasets and to validate at the tissue level. - Source: PubMed
Publication date: 2026/06/17
Li GuanpengYan XiaohaoFang Shenying - Parkinson's disease (PD) is a progressive neurodegenerative disorder in which neuroinflammation is recognized as a contributor to clinical progression. This study aimed to characterize the cerebrospinal fluid (CSF) inflammatory profile in mid- to late-stage PD patients and identify specific inflammatory proteins with potential clinical relevance to motor symptoms and disease severity. - Source: PubMed
Publication date: 2026/07/01
Guo YukunLiu WenqingBu WeitingWang RuoxiSu DaoqingLi Heng