CD226 ELISA kit
- Known as:
- CD226 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CD226-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CD226 ELISA kit
Related genes to: CD226 ELISA kit
- Gene:
- CD226 NIH gene
- Name:
- CD226 molecule
- Previous symbol:
- -
- Synonyms:
- DNAM-1, DNAM1, PTA1, TLiSA1
- Chromosome:
- 18q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-02
- Date modifiied:
- 2016-10-05
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- B7-H4, a member of the B7 family, is broadly expressed on various cancer cells and has been implicated in negative immune regulation, particularly in suppressing anti-tumor immunity. However, its receptor and the mechanisms underlying its immunosuppression remain poorly understood. Here, we identify Galectin-9 (Gal-9) as a binding partner of B7-H4 and investigate its role in modulating T cell responses. We show that glycosylation within the IgC domain of B7-H4 is required for Gal-9 binding, while the N-terminal carbohydrate recognition domain (N-CRD) of Gal-9-specifically residue R65-is essential for its binding with B7-H4. In addition, several other B7 family members (B7.1, B7.2, B7-H2, and B7-DC) and immune cell surface receptors (CD28, 2B4, CD226, and SLAMF1) also bind to Gal-9 at levels comparable to those observed with B7-H4 or TIM-3. In vitro functional assays revealed that B7-H4 inhibits Gal-9-induced activation of CD28 downstream signaling and reduces Gal-9-mediated T cell death. In vivo, Gal-9 deficiency in mice resulted in an increased proportion of splenic CD4+ T cells, whereas B7-H4 deficiency produced no detectable phenotype. Moreover, B7-H4 and Gal-9 double-knockout mice showed no additive phenotype compared with Gal-9 single-knockout mice, and tumor growth following tumor cell challenge was unaffected in all three knockout models. Collectively, these findings indicate that B7-H4, Gal-9, other B7 family members, and T cell surface immune receptors form a complex regulatory network that modulates T cell activity and anti-tumor responses, with no single component exerting a dominant effect. This study provides a detailed molecular characterization of the B7-H4-Gal-9 interaction and uncovers additional Gal-9 binding partners, offering insights into the finely tuned immune regulation mediated by the B7 family. - Source: PubMed
Publication date: 2026/09/18
Wang Ravear ZhiqiangYang FangSui Jianhua - Periodontal disease is widely recognised as a chronic infectious-inflammatory disorder, leading to the destruction of alveolar bone. Osteoclasts and their progenitors have been demonstrated to play pivotal roles in the process of periodontitis-induced bone damage. The mechanisms that govern the differentiation of osteoclasts in the context of periodontitis remain to be elucidated. In this study, we assessed the expression of CD226 on osteoclasts and their progenitors, as well as the function of CD226 in experimental periodontitis mice. Periodontitis was induced in C57BL/6 wild-type and CD226 knockout (CD226-KO) mice. Micro-CT was used to analyse bone loss. Haematoxylin-eosin (HE) or tartrate-resistant acid phosphatase (TRAP) staining was conducted to examine osteoclast differentiation. Flow cytometric analysis and quantitative real-time PCR (qRT-PCR) were used to identify the expression of CD226 and related molecules. The expression of CD226 on osteoclasts was found to decrease gradually during the process of osteoclastogenesis. In addition, the study revealed that the knockout of CD226 inhibited osteoclast differentiation in vitro. Furthermore, the knockout of CD226 has been demonstrated to attenuate inflammatory responses and alleviate bone damage in a murine periodontitis model. The present study suggests that CD226 plays an important role in regulating the function and differentiation of osteoclasts and their progenitors. The targeting of CD226 has the potential to be developed as a potent therapy for bone loss caused by periodontitis. - Source: PubMed
Publication date: 2026/09/01
Li YiZhou WenjingChen XutaoDan WenliChen LihuaZhao FangFang Liang - Anti-CD226 antibody-mediated stimulation of NK-92 cells (sNK-92) represents a potential immunotherapeutic approach; however, its cytotoxic and apoptosis-associated effects in hormone-independent solid tumors remain insufficiently characterized. This study investigated the activity of sNK-92 cells against PC3 castration-resistant prostate cancer and SH-SY5Y neuroblastoma cell lines, using PNT1A normal prostate epithelial and BJ normal dermal fibroblast cells as non-malignant controls. Cytotoxicity was assessed by CCK-8 assay at target-to-effector (T:E) ratios of 1:1, 1:5, and 1:10, and markers historically associated with the intrinsic (BAX, caspase-9), extrinsic (caspase-8), and executioner (caspase-3) apoptotic pathways were evaluated quantitatively by ImageJ-based corrected total cell fluorescence (CTCF) analysis. sNK-92 cells produced significant ratio-dependent cytotoxicity against PC3 and SH-SY5Y cells, reaching 23.76% and 26.29%, respectively, at the 1:10 T:E ratio, with sNK-92 producing significantly greater cytotoxicity than unstimulated NK-92 at this ratio in both cell lines and additionally at the 1:5 ratio in SH-SY5Y cells; no significant reduction in CCK-8 viability was detected in PNT1A or BJ cells at any ratio. Quantitative immunofluorescence analysis demonstrated substantially increased relative fluorescence intensity of all four apoptosis-associated markers in sNK-92-treated PC3 and SH-SY5Y cells compared with their corresponding controls and, in most comparisons, with NK-92-treated cells, whereas changes observed in the PNT1A and BJ non-malignant models examined were markedly smaller. These findings provide preliminary quantitative evidence that anti-CD226-stimulated NK-92 cells exert a preferential cytotoxic effect on the tumor cell models examined, relative to the non-malignant models tested, and induce changes in apoptosis-associated markers consistent with engagement of apoptotic signaling. Further orthogonal validation is warranted. - Source: PubMed
Publication date: 2026/08/25
Dastouri MohammadrezaElmusa Fatima - The COVID-19 pandemic has created a global health challenge. Severe cases are associated with immune system dysfunction, which can lead to uncontrolled inflammation. There are no published data on the specific roles of natural killer (NK)-cell subsets and immune checkpoint (IC) molecules in disease severity. Thirty-five patients diagnosed with COVID-19 and 14 healthy controls were involved in the study. From peripheral blood, CD56dim and CD56bright cell subsets were analyzed by flow cytometry for the expression of IC molecules (T-cell immunoglobulin and ITIM domain [TIGIT], CD226, and PD-1), activation markers (CD69), and cytotoxic potential (CD107a degranulation, granzymes, and perforin content). In COVID-19 patients, the proportion of CD8- CD56dim cells was significantly higher than the CD8+ subset. Inhibitory receptors TIGIT and PD-1 exhibited significantly higher relative expression in CD8+ CD56dim cells compared to their CD8- counterparts across infected groups, an effect particularly pronounced in deceased patients. Conversely, activating CD226 expression was reduced in the CD8- CD56dim subset only in severe cases. Functional assays revealed significantly elevated CD107a and CD69 expression in CD56dim cells of patients versus controls. Notably, CD8- CD56bright cells from deceased patients demonstrated enhanced CD107a expression and elevated perforin content, suggesting a shift toward hyperactivation. The preferential upregulation of inhibitory checkpoint molecules on the highly active CD8+ subset may reflect a compensatory response to immune activation, whereas the enhanced activation of CD8- NK-cell subsets was associated with disease severity and mortality. Similarly, the heightened cytotoxic profile of CD8- CD56bright cells observed in fatal cases may reflect immune dysregulation associated with severe COVID-19. - Source: PubMed
Meggyes MatyasNagy David UToth IldikoMezosi LiviaSipos DavidPeterfalvi AgnesSzereday Laszlo - The poliovirus receptor (CD155) is an emerging immune checkpoint molecule involved in the suppression of anti-tumor immunity. In ovarian cancer, CD155 is frequently overexpressed and interacts with receptors such as TIGIT, CD96, and CD226 to modulate the activity of T cells, NK cells, and dendritic cells. These interactions contribute to immune cell exhaustion, regulatory T cell expansion, and impaired cytotoxic responses, facilitating tumor immune evasion. Recent studies have revealed that CD155 expression is influenced by tumor metabolism, autophagy, and cytokine signaling. Therapeutic strategies targeting the CD155 axis-through monoclonal antibodies, bispecific constructs, or engineered T/NK cells-are being actively explored and show promise in enhancing anti-tumor responses, particularly when combined with existing checkpoint inhibitors. This review provides a comprehensive overview of the structure, function, and receptor interactions of CD155 (PVR), with a particular focus on its immunoregulatory role in the ovarian tumor microenvironment. We discuss the signaling mechanisms of the TIGIT/CD96/CD226 axis, its impact on diverse immune cell populations, and the current landscape of therapeutic strategies targeting this pathway. Finally, we evaluate the potential of CD155 and its receptors as predictive biomarkers and therapeutic targets to overcome immune resistance and improve outcomes in ovarian cancer. - Source: PubMed
Publication date: 2026/08/20
Huang MingyaoZhang JiahuiHuang HuiyanLiu LiZou Yun