Canine CD70 antigen(CD70) ELISA kit
- Known as:
- Canine CD70 antigenic(CD70) Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- e08c1493
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Blue gene shanghai
- Gene target:
- Canine CD70 antigen(CD70) ELISA kit
Related genes to: Canine CD70 antigen(CD70) ELISA kit
- Gene:
- CD70 NIH gene
- Name:
- CD70 molecule
- Previous symbol:
- CD27LG, TNFSF7
- Synonyms:
- CD27L
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-08
- Date modifiied:
- 2016-10-05
Related products to: Canine CD70 antigen(CD70) ELISA kit
Human ELC ELISA KIT 96 TEST
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Size'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(1-3)-beta-D-glucan Sandwich ELISA, Double Antibody(1-Kit )11,12-EET DHET Immunoassay Kit(1-Kit )11,12-EET_DHET Immunoassay Kit(1-Kit) 11,12-DHET Immunoassay Kit(1-Kit) 14,15-DHET Human Urine ELISA Kit(1-Kit) 14,15-DHET Hypertension ELISA Kit Related articles to: Canine CD70 antigen(CD70) ELISA kit
- Although first-line immunotherapy achieves remission in most patients with follicular lymphoma (FL), improved biomarkers and therapeutic strategies are required to identify and manage those who relapse. We investigated the immune microenvironment at diagnosis in uniformly treated FL patients with extended follow-up (>11 years), comparing relapsed and relapse-free cases. Transcriptomic profiling revealed enrichment of inflammatory response pathways in relapsed patients, including cytokine overexpression and upregulation of CD70, a molecule implicated in immune activation and inflammation. Multiplex immunofluorescence confirmed CD70 overexpression at diagnosis in tumor cells as well as in CD8⁺ and CD4⁺ T follicular helper (TFH) cells, correlating with inferior progression-free survival. Functional studies demonstrated that CD70⁺ tumor cells were more proliferative and induced CD70 expression in T cells, suggesting a feed-forward loop sustaining immune activation. To target these cells and enhance current CAR-T approaches, we engineered dual CD19-CD70 chimeric antigen receptor (CAR) T cells by co-transducing the CD19-CAR-T ARI-0001 with a CD27-based anti-CD70 CAR. Dual CAR-T cells exhibited enhanced in vitro cytotoxicity against patient-derived spheroids of FL, diffuse large B-cell lymphoma, and mantle cell lymphoma. In FL xenograft models, dual CAR-T treatment achieved superior disease control compared to monotargeted CAR-T cells, inducing complete tumor clearance in spleen and bone marrow. Collectively, these findings provide strong preclinical rationale for the clinical development of CD19-CD70 dual CAR-T therapy to improve outcomes in high-risk FL and potentially other B-cell non-Hodgkin lymphomas. - Source: PubMed
Publication date: 2026/07/22
Araujo-Ayala FerranRos MariaAlexandru RalucaMateos-Jaimez JudithRodríguez-Garcia AlbaGiménez-Alejandre MartaVillalba-Esparza MaríaMozas PabloColell GuillemColell SalutBachiller MireiaNadeu FerranRivero AndreaGiro AriadnaHodson Daniel JPoddar SoumyaLópez-Guillermo ArmandoColomer DolorsMaiques-Diaz AlbaMartín-Subero José-IgnacioBeà SilviaMagnano LauraSmith Mitchell ReedUrbano-Ispizua ÁlvaroDelgado JulioJuan ManelCampo ElíasDe Andrea Carlos EGuedan SoniaPérez-Galán Patricia - Clear cell renal cell carcinoma (ccRCC) accounts for approximately 75% of renal cell carcinomas and is defined by near-universal VHL inactivation, leading to constitutive HIF stabilisation, metabolic reprogramming, and an immunologically distinct tumour microenvironment (TME). Although ccRCC is characterised by abundant immune infiltration, this paradoxically correlates with poor prognosis, reflecting a TME that imposes interconnected physical, immunological, and metabolic barriers to effective immunotherapy. Chimeric antigen receptor (CAR)-based therapies have revolutionised the treatment of haematological malignancies, but their translation to ccRCC has encountered substantial hurdles. The first-in-human trial targeting carbonic anhydrase IX (CAIX) was limited by on-target off-tumour toxicity and CAR immunogenicity-lessons that fundamentally reshaped the field. CD70 has since emerged as the dominant clinical target, expressed in over 80% of ccRCCs with a highly restricted normal tissue distribution. The phase I COBALT-RCC trial of CTX130, an allogeneic CRISPR-Cas9-edited CD70-directed CAR-T cell product, provided formal proof of concept, achieving disease control in 81.3% of heavily pretreated patients and a durable complete response now exceeding three years-the first such sustained remission reported for any CAR-T cell product in a solid malignancy. Nevertheless, the low frequency of durable responses and universal loss of CAR-T cell persistence by day 28 underscore that major barriers remain. Beyond CD70, the field has diversified across multiple platforms, including CAR-natural killer (NK) cells, CAR-natural killer T (NKT) cells, and CAR-macrophages, each offering distinct biological advantages. This review synthesises current knowledge of the ccRCC TME, the preclinical landscape of CAR-based therapies, and emerging clinical evidence from more than 30 registered trials. We discuss target antigens; engineering strategies to overcome TME barriers, including cytokine armouring, chemokine receptor co-expression, switch receptors, and metabolic reprogramming; and rational combination approaches. We argue that the convergence of optimised target selection, cellular engineering, combination strategies, and biomarker-driven trial design may ultimately improve outcomes for patients with ccRCC. However, achieving a cure remains an aspirational goal, and significant barriers must first be overcome. - Source: PubMed
Publication date: 2026/06/24
Zhu XuyuanZhang YuChen YuxiangLi ShandaWang KunLi TaoMa XiaojieNi ZhuonaJiang Hongtao - Treatment options for clear cell renal cell carcinoma (ccRCC) refractory to immune checkpoint inhibitors (ICIs) and targeted therapy are needed. ALLO-316 is an allogeneic chimeric antigen receptor (CAR) T-cell product that targets CD70-expressing ccRCC and resists immune rejection by targeting and eliminating patients' CD70 alloreactive T cells. - Source: PubMed
Publication date: 2026/07/14
Srour Samer AChahoud JadDrakaki AlexandraCurti Brendan DGibney Geoffrey TTang LilyJiang YizhouCharmsaz SaraRobbins Paul BMcLeroy JeffSeveryn Christopher JLe Gall John BRoberts Zachary JTannir Nizar MPal SumantaKotecha Ritesh R - The clinical translation of alloantigen-specific regulatory T cells (AS-Tregs) is constrained by their low frequency in peripheral blood, limited purity, and functional instability following prolonged expansion. To address these hurdles, we developed a strategy to isolate and expand a functional CD25CD27CD70 AS-Treg population. Initially, Tregs were co-cultured with allogeneic dendritic cells in the presence of IL-15, IL-2, and retinoic acid. Proliferating CD25CD27CD70 AS-Tregs were subsequently FACS-sorted and expanded via polyclonal anti-CD3/CD28 stimulation with IL-15, IL-2, rapamycin, and TGF-β. Over three weeks, this protocol yielded a 434-fold expansion, achieving >95% purity (CD25FOXP3) while maintaining a substantial degree (>60%) of -TSDR demethylation, a hallmark of stable Treg lineage commitment. The expanded CD27 AS-Tregs exhibited a robust immunoregulatory phenotype, characterized by high expression of Helios, CTLA-4, and CD39, as well as chemokine receptors associated with allograft and lymphoid tissue homing (CXCR3, CCR4, and CCR7). Functionally, CD27 AS-Tregs suppressed T cell proliferation in an antigen-specific manner, even after exposure to inflammatory cytokines, and showed a concentration-dependent chemotactic response to CXCL10 . In addition, these cells maintained lineage fidelity by lacking the production of inflammatory cytokines such as IFN-γ and IL-17A. Accordingly, transcriptional profiling by RNA sequencing confirmed the enrichment of immunoregulatory signatures and revealed minimal changes in gene expression when expanded Tregs were exposed to inflammatory conditions. Overall, our findings suggest that CD27 AS-Tregs represent promising candidates for more stable, long-term Treg therapy to support transplant tolerance. - Source: PubMed
Publication date: 2026/06/10
Cortés-Hernández ArimelekArteaga-Cruz SaúlMartínez Iturbe Iyari IRosas-Cortina KatyaVigil Mora Marco ALegorreta-Anguiano ErickReyes Barrientos Judith EÁlvarez-Salazar Evelyn KCervera AlejandraSánchez-Hernández Beatriz EDomínguez Armando GamboaSoldevila Gloria - Immunotherapy has transformed cancer treatment; however, clinical benefit remains limited to a subset of patients, underscoring the need for robust biomarkers that capture tumor-immune interactions across cancer types. In this study, we performed a comprehensive pan-cancer, multi-omics characterization of the immune checkpoint-related molecules CD70, CD80, and TIGIT to evaluate their diagnostic, prognostic, and immunological relevance. Using integrative analyses of transcriptomic, epigenomic, genomic, pharmacogenomic, and single-cell RNA-sequencing data from The Cancer Genome Atlas and complementary resources, we assessed expression patterns, DNA methylation, somatic mutations, copy number alterations, immune infiltration, tumor stemness, and drug sensitivity. CD70, CD80, and TIGIT were broadly dysregulated across multiple malignancies, with coordinated overexpression particularly evident in kidney renal clear-cell carcinoma. Elevated expression of these immune checkpoints was associated with advanced tumor stage, aggressive molecular subtypes, and unfavorable survival outcomes in selected cancers, including uveal melanoma and renal malignancies. Functional analyses revealed significant associations between checkpoint expression and key oncogenic pathways, including epithelial-mesenchymal transition, apoptosis, and hormone receptor signaling, suggesting links with tumor progression and immune activation states. Immune deconvolution analyses indicated that TIGIT expression is associated with a T-cell-inflamed microenvironment and reduced neutrophil infiltration, while CD80 exhibited methylation-dependent associations with immune cell composition. Genomic and epigenetic alterations were found to correlate with checkpoint expression patterns and immune phenotypes across tumor types. Pharmacogenomic profiling identified associations between checkpoint expression and sensitivity to multiple anticancer agents; however, these findings are based on cell line datasets and should be considered predictive. Single-cell transcriptomic analyses further resolved cell-type-specific expression patterns, distinguishing tumor-intrinsic from immune-restricted expression profiles. Collectively, our findings establish CD70, CD80, and TIGIT as integrative biomarkers of tumor progression, immune contexture, and therapeutic response, providing a rationale for their clinical exploitation in precision immuno-oncology. - Source: PubMed
Publication date: 2026/06/21
Rigopoulos Christos PanagiotisGeorgakopoulos-Soares IliasZaravinos Apostolos