CD40L Monoclonal Antidbody [MR1]
- Known as:
- CD40L Monoclonal Antidbody [MR1]
- Catalog number:
- A-0555-500
- Product Quantity:
- 500
- Category:
- -
- Supplier:
- EpigenTek
- 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]
- Our laboratory has previously described a mouse model (CD40LΔ5) that produces 60% of wild-type CD40L due to a targeted deletion in an RNA binding site within the CD40L message. The CD40LΔ5 mutation, which destabilizes CD40L mRNA during T-cell activation, causes disrupted germinal center (GC) formation, leading to reduced levels of memory B cells and switched antibodies. In this study, we used our model of limited CD40L expression to investigate its effect on systemic lupus erythematosus (SLE, or lupus) using 2 different mouse models of SLE. The first model used the hydrocarbon oil pristane to induce lupus-like symptoms over a 6-month period, and the second utilized a chronic graft-versus-host disease (bm12-cGVHD) that resembles lupus and allowed us to monitor the early events in disease development. Importantly, we found that in both systems, female mice expressing the CD40LΔ5 mutation showed a consistent increase in elevated antibody-secreting cells and autoantibody titers. In addition, pristane-induced lupus female CD40LΔ5 mice had higher levels of immunocomplex deposition in the kidney compared to all other cohorts. Increases in autoantibodies and GC cells in female CD40LΔ5 versus wild-type recipient mice were also evident in the bm12-cGVHD model. Additionally, CD4+ T cells from female CD40LΔ5 recipient mice were skewed toward a Th2 phenotype and expressed a distinct cytokine expression pattern upon activation of dendritic cells. Overall, our results support a nuanced role for optimal CD40L expression in lupus and suggest a sex-determined threshold of CD40L-CD40 signaling that is critical at the very early steps of disease progression. - Source: PubMed
Prado De Maio DiegoTetteh SandraAyers ChristopherSt Martin AnnaBrown MichelleCovey Lori R - Platelets, classically defined by their hemostatic function, are increasingly recognized as immune effectors that shape chronic inflammation and vascular pathology in immune-mediated inflammatory diseases. In conditions such as systemic lupus erythematosus, rheumatoid arthritis, and psoriasis, immune activation skews platelet adhesion, secretion, and procoagulant activity, while persistent interferon signaling and immune complex engagement (via receptors such as FcγRIIA) amplify thromboinflammation. Platelets orchestrate leukocyte recruitment and endothelial activation through P-selectin/PSGL-1 (P-selectin glycoprotein ligand-1) interactions, CD40 ligand, interleukin-1β, and the release of extracellular vesicles carrying cytokines and RNAs. Platelet involvement manifests differently across immune-mediated inflammatory diseases. In systemic lupus erythematosus, they promote type I interferon priming, neutrophil extracellular trap formation, and endothelial dysfunction. In rheumatoid arthritis, they generate abundant synovial microparticles and systemic vascular changes. In psoriasis, they accumulate within skin lesions, enhance platelet-leukocyte aggregation and activate proatherogenic endothelial responses. These pathways promote, independent of traditional cardiovascular risk factors, atherothrombosis including myocardial infarction, stroke, and venous thromboembolism. Limited translational data suggest that hydroxychloroquine may attenuate platelet activation and improve endothelial function. P2Y inhibition may blunt interferon-linked platelet RNA signatures and leukocyte-platelet interactions. However, some therapies targeting inflammation, such as Janus kinase inhibitors, may promote thrombosis, the mechanisms of which are not fully known. Advances in multiomics, single-cell and spatial profiling, and in vivo models are delineating targets for intervention and enabling biomarker-driven risk stratification. Collectively, platelets function as central translators between autoimmunity and atherothrombosis. Defining and modulating platelet-immune crosstalk holds the potential to reduce cardiovascular risk in rheumatologic populations. - Source: PubMed
Publication date: 2026/07/28
Ni RichardBarrett Tessa JGarshick Michael S - : Left ventricular (LV) dysfunction is a clinically important complication of anthracycline- and trastuzumab-based treatment in breast cancer. Inflammatory pathways may contribute to cancer therapy-related cardiac dysfunction, and the CD40/CD40 ligand (CD40L) axis has been implicated in vascular inflammation and myocardial injury. This study assessed longitudinal changes in CD40 and CD40L during adjuvant treatment and their association with LV dysfunction. : Twenty-eight women with operable breast cancer receiving adjuvant anthracycline-based chemotherapy with or without trastuzumab were prospectively evaluated. Blood samples were collected at baseline, 6 months, and treatment completion at 15 months to measure CD40 and CD40L. Cardiac function was assessed by transthoracic echocardiography, including left ventricular ejection fraction and global longitudinal strain, at baseline and every 3 months. Repeated-measures analysis of variance examined temporal biomarker changes and interactions with LV dysfunction. : Participants had a mean age of 52.6 ± 10.7 years and a mean BMI of 25.8 ± 4.8 kg/m; 64% were postmenopausal, 76% had HER2-positive disease, and 79.3% received radiotherapy and trastuzumab. During follow-up, 15 patients (53.6%) developed LV dysfunction. CD40 levels remained stable overall ( = 0.31), whereas CD40L increased significantly over time ( < 0.001). Baseline CD40 did not differ by LV dysfunction status ( = 0.79). However, CD40 showed a significant time-by-LV dysfunction interaction ( = 0.022), increasing late in patients with LV dysfunction and declining in those without it. CD40L showed no such interaction ( = 0.85). : In this small exploratory cohort, CD40 demonstrated differential longitudinal patterns according to subsequent LV dysfunction, whereas CD40L increased over time without a clear association with LV dysfunction. These findings should be interpreted as hypothesis-generating and require validation in larger prospective cohorts. - Source: PubMed
Publication date: 2026/07/20
Efthymiou GeorgiaAnastasiou MariaOikonomou EvangelosTheofilis PanagiotisKatifelis HectorGiallafos EliasGazouli MariaKotanidou AnastasiaSiasos Gerasimos - Neuroblastoma remains one of the most lethal pediatric solid tumors, and durable control of high-risk disease is hindered not only by inefficient tumor-selective drug delivery but also by a profoundly immunosuppressive tumor microenvironment. To address these dual barriers, we developed a chemoimmunotherapeutic vesicle-mimetic platform, DAS/CD40L-EM@DOX, by engineering CD40L-overexpressing HEK-293 T donor cells, generating extracellular vesicle mimetics through extrusion, decorating the membrane with a neuroblastoma-targeting DAS peptide, and post-loading doxorubicin. The resulting formulation preserved a nanoscale vesicular morphology, displayed CD40L on the membrane, and showed favorable particle size and zeta potential characteristics. In neuroblastoma cells, DAS decoration enhanced uptake in an α7 nicotinic acetylcholine receptor-associated manner and increased the cytotoxic and immunogenic effects of doxorubicin, as evidenced by augmented apoptosis, calreticulin exposure, and HMGB1 release. In macrophage assays, CD40L-containing vesicles shifted M2-like cells toward an M1-like phenotype, increasing CD86, TNF-α and IL-6 while decreasing CD206, IL-10 and TGF-β. Functionally, this repolarization enhanced tumor-cell phagocytosis and promoted CD8 T-cell effector responses, including increased granzyme B, IFN-γ and IL-2 production. In tumor-bearing mice, DAS modification improved tumor accumulation and reduced off-target sequestration relative to unmodified vesicles. Therapeutically, DAS/CD40L-EM@DOX exerted the strongest inhibition of tumor growth, reduced tumor burden, prolonged survival, increased intratumoural M1-like macrophages and CD8 T cells, decreased M2-like macrophages and regulatory T cells, and enhanced immunogenic cell-death markers in situ. Together, these findings support DAS/CD40L-EM@DOX as a dual-function vesicle-mimetic nanomedicine that couples neuroblastoma-targeted chemotherapy with macrophage reprogramming to remodel the tumor immune microenvironment and improve antitumour efficacy. - Source: PubMed
Publication date: 2026/07/24
Wang JinkuiLuo JunyiLi JiahuiZhang ZhaoxiaTan XueWang ZhaoyinHu XiaohaiWang LiHe Dawei - Multiple sclerosis has undergone a therapeutic revolution over the past three decades. Randomized clinical trials and real-world data demonstrate that modern disease-modifying therapies substantially reduce relapse rates and acute inflammatory activity detected by magnetic resonance imaging (MRI). However, disability accumulation increasingly occurs independent of relapse activity, highlighting progression biology as the principal unmet need. Converging epidemiological and molecular evidence supports a pivotal role for Epstein-Barr virus (EBV) infection in disease initiation, whereas later stages appear dominated by brain-intrinsic mechanisms, including compartmentalized inflammation, microglial activation, failure of remyelination and accelerated biological ageing. Population-based cohorts demonstrate that early high-efficacy therapy improves long-term outcomes, yet the risk of progression rises markedly after midlife despite effective relapse suppression. Emerging biomarkers, such as serum neurofilament light chain, glial fibrillary acidic protein, paramagnetic rim lesions and advanced quantitative MRI metrics, now enable more granular monitoring of progressive pathology. Integration of imaging, fluid biomarkers, genetics and machine learning offers opportunities for individualized benefit-risk stratification. Brain-penetrant Bruton's tyrosine kinase inhibitors, CD40 ligand-targeting biologics, refined B-cell-depleting strategies and emerging chimeric antigen receptor T-cell therapies represent promising approaches to target different aspects of compartmentalized inflammation and smoldering disease biology. Future management will require mechanism-informed treatment algorithms that align therapeutic choice with dominant disease drivers while incorporating comorbidity management, de-escalation strategies and potential EBV-targeted preventive approaches to optimize outcomes across the entire disease course. - Source: PubMed
Publication date: 2026/07/21
Piehl FredrikCastelo-Branco GonçaloJagodic MajaOlsson Tomas