Anti-Mouse CD70 PE 200 ug
- Known as:
- Antibody toMouse CD70 PE 200 ug
- Catalog number:
- 12-0701-83
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD70 200
Related genes to: Anti-Mouse CD70 PE 200 ug
- 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: Anti-Mouse CD70 PE 200 ug
Related articles to: Anti-Mouse CD70 PE 200 ug
- 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 - Acute myeloid leukemia (AML) remains a highly aggressive malignancy with limited therapeutic options and poor long-term survival. A major barrier to curative treatment is the persistence of leukemic stem cells (LSCs), a chemo-resistant population that drives relapse. Chimeric antigen receptor (CAR)-T-cell therapy has transformed the treatment of B-cell hematological malignancies. However, its application in AML has been met with significant challenges. Among the key challenges are the scarcity of AML-specific antigens and the risk of on-target/off-tumor toxicity due to shared antigen expression on normal hematopoietic stem cells (HSCs) and/or mature blood cells. Early clinical trials of CAR-T-cell therapy in AML -primarily targeting CD123, CD33, or CLL‑1- have demonstrated limited durable complete remissions and/or frequent myeloablation, underscoring the need for more selective targets. While other targets show more restricted expression profiles, they are often expressed only in a small subgroup of AML patients. In this review, we systematically evaluated 63 AML-associated antigens for which CAR constructs have been reported, using five criteria: (1) homogeneous expression across AML patients, (2) uniform expression on AML cells within individual patients; (3) presence on LSCs, (4) absence on normal HSCs, and (5) no or acceptable expression on mature blood cells. Applying a 20-point scoring framework, 13 novel antigens emerged as the most promising candidates for CAR-T-cell therapy in AML: ADGRE2, SIGLEC-6, IL1RAP, MUC1, CCR1, CD155, CD70, LILRB4, GRP78, CD37, ITGB2, TIM-3 and mesothelin. We discuss the advantages and limitations of each target, along with strategies to mitigate associated risks. With no CAR-T-cell therapy currently approved for AML, this comprehensive review provides a prioritized antigen landscape and a framework to guide the rational design of next-generation CARs for this challenging malignancy. - Source: PubMed
Publication date: 2026/06/20
Van Oers FlorianFlumens DonovanHaentjens SimonKrekelbergh LaurensAnguille Sébastien - : Novel agents targeting immune checkpoints are under development to overcome resistance to PD-1/PD-L1 and CTLA-4 blockade. Incidences of immune-related adverse events (irAEs) and toxicity profiles of novel agents remain unelucidated. - Source: PubMed
Publication date: 2026/06/18
Fujiwara YuOkamura YuiRamesh MrinaliniTehrani Yasmin FakhariAburaki RionaTakahashi ToshiakiAhluwalia Manmeet SMukherjee Sarbajit - Weight loss remains one of the primary strategies for reducing cardiometabolic risk, particularly with the advent of glucagon-like peptide-1 receptor agonists, which have been demonstrated to induce significant weight loss. Recent evidence suggests, however, that weight loss does not completely normalize the underlying biology of obesity. When weight loss medications are discontinued, patients may regain lost weight along with an increase in cardiometabolic disease risk, indicating that these medications may contribute to transiently altering the phenotype of obesity, but do not produce long-term remission. Adipose tissue is increasingly recognized as an active organ regulating systemic inflammation and metabolic homeostasis. In obesity, adipose tissue becomes inflamed through the activation of innate and adaptive immune pathways. This response has a lasting effect on the immune system. T cells in adipose tissue develop memory-like qualities via epigenetic and transcriptional reprogramming and can persist after weight loss, ready for rapid activation upon renewed metabolic stress. These immunologic memory effects drive repeated weight gain, progressive metabolic dysfunction, and ongoing cardiovascular risk. An immune process is working alongside the endocrine and metabolic adjustments that facilitate energy conservation and fat regain. The repetitive cycles of weight loss and regain further amplify these responses, leading to greater inflammation. Memory T-cell populations are maintained primarily through the CD70-CD27 axis; therefore, targeting this axis may be an effective approach to developing therapies that modify immune memory and achieve long-term cardiometabolic remission when combined with weight loss. - Source: PubMed
Publication date: 2026/06/15
Sami NabeelParikh Manish AMihatov NinoSchwartzman Michal LaniadoFrishman William HPeterson Stephen J