Anti-Mouse CD96 PE 100 ug
- Known as:
- Antibody toMouse CD96 PE 100 ug
- Catalog number:
- 12-0960-82
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD96 100
Related genes to: Anti-Mouse CD96 PE 100 ug
- Gene:
- CD96 NIH gene
- Name:
- CD96 molecule
- Previous symbol:
- -
- Synonyms:
- TACTILE
- Chromosome:
- 3q13.13-q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-22
- Date modifiied:
- 2018-02-13
Related products to: Anti-Mouse CD96 PE 100 ug
Related articles to: Anti-Mouse CD96 PE 100 ug
- Papillary thyroid cancer (PTC) is the most common thyroid malignancy. Based on single-cell RNA sequencing, a previously unrecognized CD4+ T cell subset was identified, termed EGR1+CD4+ T cells. This subset produced high levels of IL-10 and IFN-γ in response to phorbol 12-myristate 13-acetate (PMA) and ionomycin, and showed distinct molecular pathway activity compared to CD4+ Tregs. CD4+ T cell-specific overexpression of EGR1 in vitro enhanced tumor cell proliferation, invasion, and migration when co-cultured with PTC cell lines. The expression profiling analysis of immune checkpoint molecules indicated that CD96 was commonly up-regulated in EGR1+CD4+ T cells, CD4+ Tregs, and other T cell subsets, especially in tumor tissues. Single CD96 blockade significantly increased the levels of IFN-γ, IL-17a, and IL-10 in EGR1+CD4+ T cells and inhibited the proliferation of PTC tumor cells. Co-blockade of CD96/TIGIT significantly enhanced the production of IFN-γ, TNF-α, and IL-17a in both EGR1+CD4+ T cells and CD3+CD4+ T cells, which also suppressed cell proliferation, invasion, and migration when co-cultured with PTC tumor cells. These findings indicated that EGR1+CD4+ T cells were a novel CD4+ T cell subset with specific functions. Single CD96 blockade or co-blockade of CD96/TIGIT enhanced antitumor immunity of EGR1+CD4+ T cells, which might be promising therapeutic strategies in PTC treatment. - Source: PubMed
Publication date: 2026/07/07
Wang ZhengshiZhang YunXu YongLiu ZhaohuiWang ShengyunYin ZhiqiangRixiati Youlutuziayi - Female patients with ERHER2 breast cancer have a favourable prognosis for 5-10 years. Later relapses are, however, common, yet predictions of late recurrence risk are suboptimal, particularly for patients with intermediate risk determined by the Oncotype Dx Recurrence Score (RS, 16-25). Here, we analyse tissue samples from patients with ERHER2 breast cancer using spatial proteomics (multiplex immunofluorescence with 5 markers, n = 440) and spatial transcriptomics (n = 359), and find decoupled immune states between stroma and epithelia. Moreover, inflamed stroma express genes linked to tissue remodelling, immune exhaustion, and inhibitory/checkpoint receptors (CTLA4, TIGIT, CD96); inflamed epithelia similarly express genes associated with checkpoints (CTLA4) and exhaustion (CXCL13), but also genes attributed to antigen presentation. In our randomised, Intermediate RS cohort treated with chemotherapy we observe an association between higher stromal tumour-infiltrating CD8 lymphocyte (sTIL CD8) density and poor outcome (ΔLR-χ: 6.79, p = 0.009), which we validate using data from whole-resection specimens (ΔLR-χ: 8.90, p = 0.003). Our data thus provide insights into the immune states in ERHER2 breast cancer, and propose sTIL CD8 density as candidate biomarker for treatment decisions. - Source: PubMed
Publication date: 2026/06/23
Kinsella ZakJahangir Chowdhury ArifNyarko Hannah NyarkoahKalinska-Lysiak DariaGonzalez Claudia AuraMurphy VerenaO'Grady TonyFay JoannaSheehan KatherineRahman ArmanCrown John PKelly Catherine MMcDade Simon SWoods InaConnolly Niamh M CPrehn Jochen H MGallagher William MO'Connor Darran P - Aging is a major driver of hematological impairment and a significant risk factor for hematologic malignancies. CD34⁺ hematopoietic stem and progenitor cells (HSPCs) represent a critical cellular compartment in which age-related changes converge to promote leukemogenesis. This review synthesizes contemporary findings on the interplay between intrinsic hallmarks of aging, including genomic instability, telomere attrition, epigenetic drift, and mitochondrial dysfunction, and extrinsic factors, including chronic inflammation and bone marrow niche remodeling, in the reprogramming of CD34⁺ cell fate. These alterations promote clonal hematopoiesis of indeterminate potential (CHIP), impair immune competence, and increase susceptibility to malignant transformation. Special attention is directed towards CD34⁺CD38⁻ subsets, which possess leukemic stem cell (LSC) functionality and demonstrate resistance to standard treatments. Emerging biomarkers, including CD123, CD96, IL1RAP, and CD133, are discussed in relation to disease progression and therapeutic targeting. We emphasize how aging-related inflammatory signaling and metabolic changes preferentially benefit pre-leukemic clones. Ultimately, we investigate therapeutic approaches designed to disrupt leukemogenesis by focusing on aging mechanisms, the senescent microenvironment, and vulnerabilities specific to leukemic stem cells (LSCs). This review contextualizes CD34⁺ cell biology within aging mechanisms, offering a cohesive view on illness onset and highlighting prospects for early intervention in older populations. - Source: PubMed
Publication date: 2026/06/11
Pandey Surya NathAfzal MuhammadRekha AVijayan Mano PriyaUniyal PrernaMaji ChandanaKhan AbidaThangavelu LakshmiNagaraj Karuppiah - Glioma is an aggressive brain malignancy characterized by a markedly immunosuppressive microenvironment and limited response to conventional treatments. CD155, also known as the poliovirus receptor, is frequently overexpressed in glioma and plays a key role in immune escape. By interacting with inhibitory receptors such as TIGIT and CD96, as well as the activating receptor CD226, CD155 modulates the tumor immune landscape. These interactions suppress the cytotoxic activity of T cells and natural killer (NK) cells while promoting immunoregulatory phenotypes, thereby impairing immune-mediated tumor cell elimination and supporting tumor progression. The balance among these receptor-ligand interactions is critical in determining immune outcomes. Targeting the CD155 axis has emerged as a potential therapeutic strategy. Approaches including monoclonal antibodies, bispecific antibodies, and chimeric antigen receptor (CAR)-engineered immune cells are being developed to counteract immune suppression and restore antitumor responses. This review summarizes the structural and functional features of CD155 and its associated receptors, examines their roles in glioma immune evasion, and discusses recent advances and challenges in developing therapies targeting this pathway. Modulation of CD155-related signaling may offer new opportunities to improve treatment outcomes in glioma. - Source: PubMed
Publication date: 2026/05/22
Huang MingyaoCui YouchenWang XiaoqianWeng YangHuang HuiyanSu WeiweiZhao ShanLi Yan - In this issue of Developmental Cell, Geng et al. show that quiescent persister tumor cells (PTCs) in colorectal cancer are enriched after neoadjuvant chemotherapy and exhibit increased expression of CD155, leading to dysfunction of tumor-infiltrating CD96CD8 T cells. Anti-tumor activity can be restored through CD96-targeted monoclonal antibody therapy. - Source: PubMed
Gorol Johanna MGreten Florian R