Anti-Mouse CD8a PE 500 ug
- Known as:
- Antibody toMouse CD8a PE 500 ug
- Catalog number:
- 12-0081-85
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD8a 500
Related genes to: Anti-Mouse CD8a PE 500 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-Mouse CD8a PE 500 ug
Related articles to: Anti-Mouse CD8a PE 500 ug
- Köhlmeier-Degos disease (Degos disease [DD]) is a rare vasculopathy with characteristic skin lesions and life-threatening gastrointestinal and cerebrovascular involvement. Although DD is often viewed as a thrombo-obliterative disorder, its immunopathology remains poorly defined. Here, single-cell RNA and T cell receptor sequencing of skin, blood, and cerebrospinal fluid from DD patients reveal pervasive type I and type II interferon activation, with an interferon-γ-biased program compared with systemic lupus erythematosus. Cytotoxic CD8A T cells show interferon-responsive activation and restricted clonotypic diversity, implicating cellular immunity in the DD inflammatory landscape. In a single-patient interventional study, JAK inhibition with ruxolitinib is associated with suppression of interferon-responsive programs, improvement of cutaneous inflammation, and stabilization of neurological disease. These findings support DD as an interferon-driven inflammatory vasculopathy and provide a rationale for further evaluation of interferon-JAK-STAT signaling. This study has been registered at ClinicalTrials.gov (NCT05998395). - Source: PubMed
Publication date: 2026/07/30
Cudrici Cornelia DGoel ShubhamSakamoto KeikoJin Seon-PilSekiguchi AkikoRosing Douglas RHuffstutler RebeccaHammoud Dima AShapiro LeeSchwartz Daniella MManohar-Sindhu SahanaTaylor Monica EZhang YueSchaughency PaulCowen Edward WHasni SarfarazKaplan Mariana JKong Heidi HBoehm ManfredNagao Keisuke - Lung squamous cell carcinoma (LUSC) frequently metastasizes to lymph nodes, yet how tumor-intrinsic biomechanical cues influence nodal immune environments remains unclear. Here, we identify solid stress, generated during tumor expansion, as a key driver of pre-metastatic niche formation in tumor-draining lymph nodes (TDLNs). Using murine models with defined solid stress levels, we show that high-stress tumors induce early TDLN remodeling characterized by fibroblast activation and accumulation of immunosuppressive S100a8⁺ myeloid cells. Single-cell and spatial transcriptomics reveal that Col1a1⁺ fibroblasts upregulate STAT3 and YAP-dependent chemokines (CCL2, CSF1), establishing a fibroblast-myeloid signaling axis that supports myeloid recruitment and suppresses CD8⁺ T cell infiltration. Functional blockade of CCR2, CSF1R, STAT3, or YAP disrupts fibroblast-myeloid co-localization, restores antigen-presenting cell populations, and enhances CD8⁺ cytotoxic T cells activity, leading to reduced lymph node metastasis and improved survival. Mechanistically, chromatin accessibility and ChIP assays reveal direct binding of p-STAT3 and YAP at inflammatory enhancer elements in fibroblasts under mechanical strain. Cross-species spatial transcriptomic analysis confirms the inverse association between Col1a1⁺ fibroblast density and CD8A⁺ T cell presence in human LUSC tissues. Our findings uncover a mechano-immune circuit whereby tumor-derived solid stress activates fibroblast-STAT3/YAP signaling to remodel TDLNs into immunosuppressive, metastasis-permissive niches. Targeting this biomechanical axis offers a promising strategy to intercept early lymphatic dissemination in LUSC. - Source: PubMed
Publication date: 2026/06/17
Cai JieAn ZhaoGao WeiLi RyanChen Zhe-ShengLi AnZhu LeiShen Yingran - BackgroundIncreasing evidence shows that, compared with the general population, the prevalence of coronavirus disease 2019 is significantly higher in patients with psoriasis treated with immunosuppressive therapy. However, the underlying mechanisms have not yet been clarified.Materials and methodsThe aim of this study was to further investigate the molecular mechanisms underlying these two diseases. Gene expression profiles for coronavirus disease 2019 and psoriasis were downloaded from the gene expression omnibus database (GSE150316 and GSE30999). After identifying the common differentially expressed genes between coronavirus disease 2019 and psoriasis, functional annotation, protein-protein interaction network analysis, module construction, and hub gene identification were performed. Finally, transcription factor-gene regulatory and transcription factor-miRNA regulatory networks of the hub genes were constructed.ResultsA total of 306 common differentially expressed genes, including 168 upregulated genes and 138 downregulated genes, were identified and used for subsequent analysis. According to Kyoto Encyclopedia of Genes and Genomes enrichment analysis, the Rap1 signaling pathway, axon guidance, and focal adhesion contribute to the occurrence and development of coronavirus disease 2019 and psoriasis. Finally, five hub genes, namely EGF, IL1B, SERPINA1, CD8A, and WNT5A, were identified using the CytoHubba plug-in. Among them, three hub genes (EGF, SERPINA1, and CD8A) showed good diagnostic marker value for coronavirus disease 2019 and psoriasis.ConclusionOur findings suggest that coronavirus disease 2019 and psoriasis share common molecular mechanisms that are driven by several specific hub genes. This study provides new insights into the relationship between coronavirus disease 2019 and psoriasis. - Source: PubMed
Publication date: 2026/07/28
Zhang YuanyuanXie XiDai TingtingLi WeiZhang Wen - Biomarker discovery in sarcoidosis mechanisms represents an innovative research tool. Inflammatory responses in sarcoidosis patients were analyzed by flow cytometry to highlight CD8a+CD45+, CD45+CD8a-, CD4+CD19+, CD4+CD19-, CD3+CD56+CD16+, CD56+CD16+, and CD16+CD56- as predictive biomarkers. In our study, monocyte-derived macrophage activation (M1 phenotype), represented by CD8a+CD45+ expression, is characteristic of granulomatous inflammation in active and progressive sarcoidosis and serves as a biomarker with very good accuracy and high specificity for establishing a diagnosis of sarcoidosis. As a prognostic biomarker, it is an independent predictive factor of disease progression, being negatively associated with applied treatments by sarcoidosis stage. The accumulation of activated CD4+ T-helper cells in sarcoid granulomas is responsible for the establishment of a pro-inflammatory phenotype and serves as a biomarker with good accuracy and high specificity for sarcoidosis diagnosis. As a prognostic biomarker, CD3+CD56+CD16+ (iNKT) is an independent predictor associated negatively with disease progression, being positively correlated with treatment applied by sarcoidosis stage. CD biomarker analysis, yielding predictive models with specificity for diagnosis and prognosis, is an important research tool for estimating disease progression in patients with different inflammatory response phenotypes across the stages of sarcoidosis. - Source: PubMed
Publication date: 2026/07/22
Matei ElenaPîslan Zamfir VioricaȘuța Victoria-CristinaCozaru Georgeta CameliaDanteș Elena - Heat stroke is the most severe heat-related illness, characterized by an inflammatory response, oxidative stress, ferroptosis, and immune dysfunction. However, the broader role of ferroptosis in the pathophysiological processes of heat stroke remains unclear, and its potential connection with immune regulation has not yet been fully elucidated. This study uses bioinformatics analysis of heat stress datasets and molecular validation in patient samples to investigate key signaling pathways altered in heat stress (GSE90763) and validate their associations in heat stroke patients, aiming to clarify their connections with ferroptosis and immune regulation. - Source: PubMed
Publication date: 2026/07/17
Cui QiXu ZhongyanLei DaxinYu ChaoLuo YulingZheng JieWang Fukun