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]
- To characterise early treatment-associated changes in circulating immune mediators following sirolimus initiation in patients with tocilizumab-resistant idiopathic multicentric Castleman disease (iMCD). - Source: PubMed
Publication date: 2026/08/14
Koga TomohiroFukui ShoichiSumiyoshi RemiShimizu ToshimasaHosogaya NaokiFukushima ChizuYamamoto HiroshiYoshifuji HajimeHiga ShinjiKawakami Atsushi - Visceral leishmaniasis (VL), caused by Leishmania donovani, is characterized by progressive immune dysregulation that supports parasite persistence. The CD40-CD40L axis is essential for antigen-presenting cell (APC) licensing and Th1-mediated nitric oxide-dependent parasite control; however, how its function evolves during infection remains incompletely understood. Here, we define the temporal regulation and functional polarity of CD40 signalling during experimental VL. Using BALB/c mice and primary macrophage assays, we investigated the temporal regulation of CD40 signalling during experimental VL. CD40 expression, cytokine production, nitric oxide levels, antibody responses, T-cell phenotypes, immune checkpoint expression, and macrophage activation were evaluated during progressive infection. Functional studies included CD40 agonism, CD40 knockdown, and TRAF-selective CD40 reconstitution to assess stage-specific effects on parasite control and immune regulation. Increasing parasite burden drove a gradual shift in CD40 signalling from protective to suppressive outcomes. In vitro infection reduced CD40 expression and IL-12 production while increasing IL-10, indicating early impairment of APC licensing. In vivo, progressive splenic infection was associated with diminished nitric oxide production, a declining IgG2a/IgG1 ratio, expansion of GATA3+ Th2 and FOXP3+ regulatory T-cell populations, and increased PD-L1 and TIM-3 expression, consistent with a regulatory and exhausted immune environment. Despite partial recovery of CD40 expression on myeloid APCs at later stages, declining CD40L+ T-cell availability and sustained IL-10/Arg1 signalling limited functional responsiveness. Early CD40 agonism failed to restore parasite control, whereas late activation exacerbated disease. CD40 knockdown increased parasite burden and reduced iNOS+ macrophages, confirming the requirement for CD40-dependent licensing. Finally, TRAF2-biased CD40 signalling promoted macrophage activation and parasite restriction, whereas TRAF6-biased signalling reinforced immunosuppression. These findings identify a stage-dependent functional threshold beyond which CD40 signalling no longer sustains protective immunity during VL, highlighting the importance of restoring APC competence and selectively directing CD40 signalling through TRAF2-linked pathways. - Source: PubMed
Mahor HimaSaha Bhaskar - 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