CD40L Monoclonal Antidbody [MR1]
- Known as:
- CD40L Monoclonal Antidbody [MR1]
- Catalog number:
- a-0555-500
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Epigentek inc
- Gene target:
- CD40L Monoclonal Antidbody [MR1]
Related genes to: CD40L Monoclonal Antidbody [MR1]
- Gene:
- AATK NIH gene
- Name:
- apoptosis associated tyrosine kinase
- Previous symbol:
- -
- Synonyms:
- AATYK, KIAA0641, LMTK1, LMR1, AATYK1, PPP1R77
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-16
- Date modifiied:
- 2016-06-29
- Gene:
- ADGRE1 NIH gene
- Name:
- adhesion G protein-coupled receptor E1
- Previous symbol:
- TM7LN3, EMR1
- Synonyms:
- -
- Chromosome:
- 19p13.3-p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-08-31
- Date modifiied:
- 2018-02-13
- Gene:
- ATP2C1 NIH gene
- Name:
- ATPase secretory pathway Ca2+ transporting 1
- Previous symbol:
- BCPM
- Synonyms:
- KIAA1347, ATP2C1A, PMR1, SPCA1
- Chromosome:
- 3q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-19
- Date modifiied:
- 2016-10-05
- 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
- Gene:
- FAN1 NIH gene
- Name:
- FANCD2 and FANCI associated nuclease 1
- Previous symbol:
- KIAA1018, MTMR15
- Synonyms:
- -
- Chromosome:
- 15q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-10-28
- Date modifiied:
- 2016-12-21
Related products to: CD40L Monoclonal Antidbody [MR1]
Related articles to: CD40L Monoclonal Antidbody [MR1]
- Systemic lupus erythematosus (SLE) is a heterogeneous systemic autoimmune disease, yet the molecular basis underlying this variability remains incompletely understood. We profiled the plasma proteome in 260 SLE patients and 86 healthy volunteers (HVs) using the SomaScan v4.1 platform, quantifying 7,288 analytes corresponding to 6,595 unique proteins. We identified 215 proteins that were robustly differentially abundant between SLE patients and HVs in both discovery (n=207 SLE, n=45 HVs) and validation sets (n=53 SLE, n=41 HVs). Within-cases analyses identified 421 proteins associated with disease activity. Network-based clustering delineated correlated protein modules, including an interferon-associated module and a renal-associated module. Autoantibody-stratified analyses further uncovered distinct proteomic endotypes: positivity for antibodies targeting RNA-binding proteins (anti-Sm, anti-Ro-60, anti-RNP68, anti-RNP-A) was associated with increased interferon-stimulated protein levels (e.g., MX1, ISG15, CXCL10), independent of disease activity. Anti-Sm, anti-RNP-A and anti-Ro52 antibodies were associated with reduced plasma levels of their respective autoantigens. Anti-dsDNA antibodies were associated with elevated levels of CD40 ligand (CD40LG) and the neutrophil protease proteinase-3. Moreover, we identified an association between CD40LG and disease activity specific to the anti-dsDNA positive subgroup. Together, these data define plasma protein signatures of SLE and disease activity, highlight autoantibody-specific molecular phenotypes, and provide a basis for precision medicine. - Source: PubMed
Publication date: 2026/06/02
Leung Geoffrey H DBottomley CharlotteBuang NorzawaniMaughan Robert TWhittle Benjamin JZeidaabadi BoroumandHuang Yun-JuTurner-Stokes TabithaCondon MarieLightstone LizCairns TomBotto MarinaPickering Matthew CPeters James E - The receptors of the tumor necrosis factor (TNF) receptor superfamily (TNFRSF) are of overwhelming scientific and clinical relevance and stand at the center of intensive basic and translational research efforts. TNFRSF receptors (TNFRs) are engaged by membrane-bound ligands of the TNF superfamily (TNFSF) and, in some cases, by soluble ligand molecules released from the membrane-bound TNFSF ligand (TNFL) molecules. The development of recombinant TNFL-based TNFR agonists for research and especially therapeutic purposes is highly "individualized", as ligand type-specific hurdles must be overcome in terms of stability, manufacturability, TNFR-specificity and need for oligomerization. TNFR-specific antibodies can also show agonistic activity, but this agonism typically requires FcγR-binding, resulting in a reciprocal conditional bispecific FcγR/TNFR agonism not useful for the study or exploitation of pure TNFR agonism. Some antibodies trigger intrinsic TNFR agonism independent from FcγR-binding, but the rational development of such antibodies is poorly predictable and furthermore challenging due to isotype- and epitope-requirements and poor specific activity when benchmarked with FcγR-bound anti-TNFR antibodies.Using a series of nanobodies (or single-domain antibodies (sdAbs) or variable heavy domain of heavy chains (VHHs)) specific for the TNFRSF members 41BB, BCMA, CD40, CD95, TRAILR2/DR5, GITR, OX40, TNFR1 and TNFR2, we show here that genetic fusion of single-chain encoded triplets of these nanobodies with oligomerizing protein scaffolds regularly results in potent hexa-, nona- and dodecavalent agonists inducing TNFR signaling with EC50-values in the sub-nanomolar range. The oligovalent nanobody formats described exhibit superior CMC properties and enable the simple generation of highly active TNFR agonists from virtually any TNFR-specific nanobody. - Source: PubMed
Publication date: 2026/05/30
Lang IsabellZaitseva OlenaGlöckler AmelieSiegmund DanielaSheta DaliaMouhandes BayanWeisenberger DanielaSchäfer ViktoriaStepanzow SvetlanaSchneider TheresaBeilhack AndreasCrauel AlexanderKilisch MarkusFunk Lisa-MarieGötzke HansjörgFrey SteffenWajant Harald - 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