Rabbit Anti-Human CD273
- Known as:
- Rabbit Antibody toHuman CD273
- Catalog number:
- 129-10135
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rabbit Anti-Human CD273
Related genes to: Rabbit Anti-Human CD273
- Gene:
- PDCD1LG2 NIH gene
- Name:
- programmed cell death 1 ligand 2
- Previous symbol:
- -
- Synonyms:
- PD-L2, Btdc, PDL2, bA574F11.2, CD273, B7-DC
- Chromosome:
- 9p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-14
- Date modifiied:
- 2016-10-05
Related products to: Rabbit Anti-Human CD273
Related articles to: Rabbit Anti-Human CD273
- Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint inflammation and destruction. Identifying novel therapeutic targets is crucial for improving RA treatment. This study aimed to identify immune-related biomarkers in RA and investigate the potential of CD27 as a therapeutic target. We employed bioinformatics analysis of gene expression data from RA patients and healthy controls (GSE55457), followed by machine learning approaches (LASSO regression and Boruta algorithm) to identify potential biomarkers. Findings were validated in an independent dataset (GSE55235). The therapeutic potential of CD27 neutralization was evaluated in a collagen-induced arthritis (CIA) mouse model. Mechanisms were explored through quantitative real-time PCR, Western blot analysis, ELISA, and flow cytometry to assess T cell subsets, cytokine profiles, and signaling pathways. Bioinformatics analysis identified 714 differentially expressed genes, and machine learning analyses identified CD27, CD24, TNFRSF4, and PDCD1LG2 as potential RA biomarkers, all demonstrating strong diagnostic performance. CD27 showed significant positive correlations with T lymphocyte infiltration. In the CIA model, CD27 neutralization significantly reduced arthritis severity scores. This therapeutic effect was associated with suppression of Th1 responses, evidenced by significantly decreased serum levels of Th1 cytokines (IFN-γ, IL-2, TNF-α) and reduced CD4 + IFN-γ + cell populations, while Th2-related cytokines (IL-4, IL-5) remained largely unaffected. Mechanistically, CD27 neutralization attenuated phosphorylation of AKT and NF-κB p65 in vivo, while p38 MAPK remained unchanged. In vitro, recombinant CD27 protein stimulation of naive CD4 + T cells promoted Th1-biased differentiation, increasing CD4 + IFN-γ + cells and enhancing the phosphorylation of NF-κB p65 and AKT. Our study identifies CD27 as a potential therapeutic target in RA. CD27 neutralization attenuates arthritis severity by suppressing Th1 responses, possibly through modulation of AKT and NF-κB signaling pathways. These findings provide new insights into RA pathogenesis and suggest CD27 as a promising target for RA treatment. - Source: PubMed
Publication date: 2026/04/25
Lu AnghanPu LuqiaoTian YadanSong JiaxinLuo DingxiaWu Jingjin - A 52-year-old man presented with sarcomatoid diffuse pleural mesothelioma that had relapsed at an isolated site after a complete response to dual-immune checkpoint inhibition (ICI). Targeted sequencing exhibited amplification of chromosome 9p24, encompassing JAK2, PD-L1, PD-L2, and PTPRD in the relapsed (post-ICI) tumor, compared with baseline (pre-ICI). On multiplex immunofluorescence, tumor-associated macrophages (TAMs) and CD8 cytotoxic T lymphocytes (CTLs) made up most of the cells in baseline and relapsed tumor (59% and 47%, respectively). Baseline tumor cells expressed genes linked to extracellular matrix remodeling and epithelial-mesenchymal transition, intermixed with M2-like TAMs and tissue-resident, effector-like CTLs. Relapsed tumor cells shifted to a growth factor-driven phenotype (NT5E, NOD1, GATA2, FN1, PDCD1LG2) that is known to cause functional impairment of CTLs, which then transitioned to an exhausted state (FCRL3, CST7, GPR171, TRAT1, LAG3); exhausted CD8 and CD4 T cells are seen in the peripheral blood at relapse. TAMs were enriched in antigen-presentation (CD80, CD86, CXCL10), extracellular matrix-degradation (MMP9, CTSL), and CTL-suppression (ARG1, PLA2G7) pathways. Our analyses revealed that regional immunosuppression mediated by adaptive reprogramming of tumor-cell and immune-cell (TAMs, CTLs)-intrinsic changes-rather than by immune evasion or stromal exclusion-served as a mechanism of acquired resistance to dual-ICI therapy. - Source: PubMed
Publication date: 2026/04/15
Ollila HelyKulkarni PrateekKim HyojinAnkola PratitiChintala Navin KThomas CarlosSauter Jennifer LOffin MichaelAdusumilli Prasad S - Bladder cancer is one of the most common urological malignancies, with 5-year survival rates below 40% in advanced cases. Oncologic immunotherapy has become a popular approach to treating cancer and programmed death ligand 1 (), programmed death ligand 2 (), intercellular adhesion molecule 2 () and 4-1BB ligand () are key costimulatory molecules in oncologic immunotherapy. Previous research has shown plant phytochemicals can act as immunomodulators by regulating costimulatory functions to increase T-cell activation and thus to inhibit malignant proliferation. However, the role of in the growth of bladder cancer and in the expression of these key costimulatory molecules has not been elucidated yet. This study is designed to investigate if could have a role in the growth of bladder cancer and if it has any effect on the expression of these key costimulatory molecules in bladder cancer. - Source: PubMed
Gutiu Arturo GMarrah Austin JVoss Brady BCowan Braydon CMayberry Trenton GWakefield Mark RFang Yujiang - Macrophages play a pivotal role in modulating immune responses in connective tissue disease-associated interstitial lung disease (CTD-ILD). The role of programmed death ligand-2 (PD-L2), an immune checkpoint molecule expressed on macrophages, in macrophage polarization in CTD-ILD remains poorly understood. Serum PD-L2 levels were measured in CTD-ILD patients, CTD-nonILD patients, and healthy controls. Alveolar macrophages (AMs) were transfected with PD-L2-targeting shRNA or control constructs, and their effects on macrophage phenotype and fibroblast fate were evaluated. M1/M2 polarization was assessed by RT-PCR, Western blotting, and flow cytometry. Human embryonic lung fibroblasts (HELFs) were co-cultured or treated with macrophage-conditioned media, and assays for cell viability, apoptosis, fibrosis, and ferroptosis were performed. A bleomycin (BLM)-induced CTD-ILD mouse model was used to evaluate the effects of PD-L2 knockout on lung fibrosis and ferroptosis markers. Serum PD-L2 levels were significantly lower in CTD-ILD patients compared with CTD-nonILD patients and healthy controls, and negatively correlated with the extent of lung fibrosis. In vitro, PD-L2 knockdown in AMs promoted M1 polarization, suppressed M2 related markers, and induced fibroblast apoptosis, fibrosis, and ferroptosis. Conditioned media from PD-L2-deficient macrophages produced similar effects. In vivo, PD-L2 knockout mice exhibited decreased numbers of CD206 macrophages and regulated ferroptosis markers (ACSL4 upregulation, GPX4 and FTH1 downregulation) in lung tissues following BLM treatment. This study identifies PD-L2 as an important regulator of macrophage polarization and fibroblast responses in CTD-ILD. Our findings suggest that serum PD-L2 levels may reflect disease severity, and that restoring PD-L2 function could represent a potential therapeutic direction warranting further investigation in preclinical models. - Source: PubMed
Publication date: 2026/03/13
Lu JunhuiFeng XiuyuanChang XinCheng WeiPan PengfeiWu Jian - Endometrial cancer (EC) is an important health issue among women, with immunotherapy emerging as a promising option for advanced cases. Tumor-infiltrating lymphocytes (TILs) and immune checkpoints, including , , and , are increasingly recognized as prognostic markers. This study aimed to construct an immune network and assess the prognostic impact of checkpoint genes in EC using STRING, MCODE, and GEPIA2. - Source: PubMed
Publication date: 2026/03/01
Ribeiro DA Costa Rafael Everton AssunçãoZeferino Luiz CarlosTeixeira Júlio César