CD154 antibody (Azide Free)
- Known as:
- CD154 (anti-) (Azide Free)
- Catalog number:
- 10r-cd154dmsp
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- CD154 antibody (Azide Free)
Ask about this productRelated genes to: CD154 antibody (Azide Free)
- Gene:
- CD40LG NIH gene
- Name:
- CD40 ligand
- Previous symbol:
- HIGM1, IMD3, TNFSF5
- Synonyms:
- CD40L, TRAP, gp39, hCD40L, CD154
- Chromosome:
- Xq26.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-04-23
Related products to: CD154 antibody (Azide Free)
Related articles to: CD154 antibody (Azide Free)
- Dapirolizumab pegol is a novel CD40 ligand inhibitor. In this phase 3 trial, we aimed to evaluate the efficacy and safety of dapirolizumab pegol in patients with systemic lupus erythematosus (SLE). - Source: PubMed
Publication date: 2026/05/29
Clowse Megan E BIsenberg David AMerrill Joan TDörner ThomasPetri MichelleVital Edward MMorand Eric FTouma ZahiAskanase Anca DIoannou YiannisBrookes StephenGaiha-Rohrbach JanineKoch E DietlindZibian NourMartin ChristopheJimenez TeriNelde AnnetteStach Christian - Glioblastoma (GBM) is the most aggressive primary brain tumor with extremely poor prognosis. Conventional diagnostic and prognostic approaches remain inadequate, highlighting the need for integrative strategies to improve patient outcomes. We analyzed ligand-receptor (L-R) interactions in TCGA-GBM transcriptomes using BulkSignaL-R, and validated their spatial expression patterns with single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics datasets. Prognostic histopathological features were extracted from hematoxylin and eosin (H&E)-stained sections through omics-guided feature identification, followed by classification using machine learning algorithms. We identified four pivotal L-R pairs (LTB-CD40, VEGFA-ITGB1, FN1-COL13A1, and TGM2-ITGB1) to construct a risk model, which served as an independent prognostic factor for overall survival. The multivariate Cox regression analyses revealed that the risk score was significantly associated with Overall Survival (OS) (HR = 1.67, 95% CI: 1.25-2.25, < 0.001). High-risk patients exhibited distinct molecular signatures, including CALN1 mutations, specific CNV patterns, and enriched Notch/interferon-γ signalings. scRNA-seq and spatial transcriptomics revealed that these L-R pairs were predominantly expressed in gMES-like glioma cells, OPC-like cells, and pericytes. Finally, our deep learning model successfully stratified risk groups based on histological features, identifying specific tumor regions (Clusters 0, 2, 4, and 5) as critical determinants of prognosis (AUC = 0.750 by Logistic Regression). We developed a novel multi-modal framework integrating L-R interactomics and deep learning-based pathomics. This approach not only elucidates the molecular and spatial landscape of glioma intercellular communication but also provides a methodological framework for risk stratification. - Source: PubMed
Publication date: 2026/05/14
Gao LunZhang RuiZhu XiaonanXu HaitaoChen QianxuePeng MinLiu Junhui - Restoring antigen-specific immune tolerance remains a central challenge in the treatment of autoimmune diseases, as conventional immunosuppressive therapies lack specificity and can compromise protective immunity. Tolerogenic dendritic cell (tolDC) therapies offer a promising strategy for inducing durable, antigen-specific regulatory T cell (Treg) responses, but current methods for generating tolDCs are limited by poor longevity and Treg generative capacity. This study evaluates the clinical potential of Push/Pull Immunomodulation (PPI), a novel combinatorial approach identified through high-throughput molecular screening, in human monocyte-derived dendritic cells (moDCs). The phenotype, cytokine profile, and longevity of PPI-treated moDCs were benchmarked against conventional tolDC induction agents. Functional assays assessed the capacity of PPI-tolDCs to induce antigen-specific Tregs. PPI-treated moDCs exhibited increased expression of tolerogenic markers (interleukin-10, programmed cell death receptor ligand 1, and B- and T-lymphocyte attenuator), enhanced in vitro longevity, and a unique transcriptomic signature characterized by upregulation of IDO1, IDO2, and T cell-sustaining cytokines. Notably, PPI9 induced robust, antigen-specific Treg responses, suggesting the potential for long-term tolerance induction. Although transient tumor necrosis factor-α release and moderate upregulation of CD40 and CD86 were observed, these did not impair Treg generation, indicating that PPI-tolDCs overcome key barriers associated with conventional tolDC therapies. PPI enables the generation of stable, long-lived human tolDCs with superior capacity to induce antigen-specific Tregs. Ongoing studies will further explore the translational potential of PPI-tolDCs for clinical applications in autoimmunity and transplantation. SIGNIFICANCE STATEMENT: This study validates a novel molecular combination to generate tolerogenic dendritic cells with primary human cells. These tolerogenic dendritic cells have potential use as a cell therapy for autoimmune diseases and transplantation. - Source: PubMed
Publication date: 2026/04/24
Jia SihanMell JoshuaDeak Peter - Recessive dystrophic epidermolysis bullosa (RDEB) is a devastating genodermatosis caused by biallelic mutations, where chronic inflammation drives disabling complications affecting quality of life and survival. Effective inflammatory control remains a major unmet need. While systemic administration of mesenchymal stromal cells (MSC) from various sources has proven safe with transient benefits yet only one recent placebo-controlled study in RDEB. Consistent type VII collagen (C7) deposition is lacking, and therapeutic mechanisms and predictive biomarkers remain undefined. The MesenSistem-EB trial evaluated for the first time the use of haploidentical BM-MSC and extensively explored their anti-inflammatory potential as a monotherapy in RDEB. - Source: PubMed
Publication date: 2026/05/05
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Publication date: 2026/05/13
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