CD8A_HUMAN CD8A ELISA tesk kit
- Known as:
- CD8A_HUMAN CD8A Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen13470
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- CD8A_HUMAN CD8A ELISA tesk kit
Related genes to: CD8A_HUMAN CD8A ELISA tesk kit
- 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: CD8A_HUMAN CD8A ELISA tesk kit
Related articles to: CD8A_HUMAN CD8A ELISA tesk kit
- Cyclophosphamide is widely used in oncology, autoimmune disorders, and transplantation-related conditioning or post-transplant immunosuppression. However, its therapeutic value is limited by hematopoietic and lymphoid toxicity, including leukopenia, neutropenia, anemia, thrombocytopenia, bone marrow suppression, thymic injury, and prolonged impairment of T-cell recovery. These effects may occur after pulsed intravenous administration, high-dose regimens used in transplantation or severe refractory disease, and continuous low-dose/metronomic exposure. Therefore, there is a medical need for pharmacological agents capable of compensating cyclophosphamide-induced hematopoietic and lymphopoietic suppression without causing uncontrolled stimulation of early progenitor cells. - Source: PubMed
Publication date: 2026/08/03
Ten AsselBaktybayeva LayilyaKoshetova ZhanargulKoizhaiganova RaushanDaulet GuldanaZharkynbek TolganayYu Valentina - Adjuvants are critical for enhancing vaccine efficacy, however, conventional adjuvants often suffer from poor biocompatibility and limited immune activation profiles. Herein, we developed a nanoadjuvant by modifying a lentinan (LNT) backbone with polyethyleneimine (PEI) to generate a cationic LNT-PEI vector, which was then used to load SOCS1 siRNA, forming LNT-PEI/siRNA nanocomplexes. experiments demonstrated that LNT-PEI/siRNA effectively silenced gene expression, significantly upregulated the expression of CD80 and CD86, and promoted the secretion of TNF-α and IL-6. Furthermore, a vaccine was formulated by self-assembling the LNT-PEI/siRNA nanoadjuvant with the model antigen ovalbumin (OVA) to evaluate its immunostimulatory capacity. Biodistribution studies revealed that the vaccine formulation effectively targeted and accumulated in lymph nodes while reducing non-specific hepatic retention. Immunological evaluation showed that incorporation of LNT-PEI/siRNA markedly increased the proportions of CD11bF4/80 macrophages and CD11c dendritic cells, as well as CD3CD8a T cells in the spleen. It also upregulated costimulatory molecule expression and elevated serum levels of TNF-α, IL-6, and IFN-γ. In summary, the LNT-PEI/siRNA nanoadjuvant developed in this study successfully enhances immune responses, providing both a theoretical foundation and experimental basis for the development of next-generation vaccine adjuvants. - Source: PubMed
Publication date: 2026/08/14
Zhu YingShen YaoyanBao YumengMei CongjinZhou JuanChen Jinghua - 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