Human CD40L ELISA Kit
- Known as:
- Human CD40L Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 55r-1711
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- Human CD40L ELISA Kit
Related genes to: Human CD40L ELISA Kit
- 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: Human CD40L ELISA Kit
Related articles to: Human CD40L ELISA Kit
- Long-term survival of lung transplant recipients remains limited by chronic lung allograft dysfunction (CLAD). CLAD is only diagnosed following a persistent and substantial decline in lung function, after which irreversible damage to the lungs has occurred, limiting opportunities to effectively intervene at an early stage. There is a critical need for earlier detection prior to its clinical manifestation. The immunological drivers of CLAD remain unclear, limiting the development of predictive biomarkers and new therapies. - Source: PubMed
Publication date: 2026/06/23
Iacono GiuliaBegka ChristinaCardwell BaileyDaunt CarmelChatzis RoxannePattaroni CelineButler AlanaMacowan MatthewLevvey BronwynSnell Gregory IWestall Glen PMarsland Benjamin J - Dendritic cells (DC) play a central role in host immunity as they carry environmental cues from sites of infection to the lymphatics, where they subsequently direct appropriate adaptive immune responses. Importantly, this process is exploited by pathogens such as HIV-1, which utilize DC to efficiently facilitate HIV-1 -infection of CD4 T cells. In this study, we show that monocyte-derived DC matured under type-1 proinflammatory conditions, either through exposure to soluble mediators of type-1 immunity or through bystander activation of cytotoxic T cells, display enhanced -infection capacity, while prostaglandin E2 exposure diminishes this trait. This heightened -infection activity involves DC upregulation of sialic acid binding immunoglobulin-like lectin-1 (Siglec-1/CD169) surface expression and a distinct responsiveness to the CD4 T helper cell signal CD40L. The upregulated expression of Siglec-1 increases HIV-1 surface binding potential on these proinflammatory DC, while CD40L/CD40 signaling uniquely induces the formation of pronounced morphologic extensions and the release of the chemokine CCL20, together increasing CD4+ T cell access and susceptibility to HIV-1 infection. Overall, this study demonstrates that the nature of environmental signals received by monocyte-derived DC during maturation and the character of their subsequent responsiveness to CD40L-expressing T helper cells dictates their ability to facilitate HIV-1 -infection. - Source: PubMed
Publication date: 2026/06/04
Bothwell E GraceDePuyt Allison EZaccard Colleen RAnderko Renee RShoucair Peter E JBilben Holly AGarcia-Bates Tatiana MGerberick Abigail DWatkins Simon CSluis-Cremer NicolasRinaldo Charles RMailliard Robbie B - Poxvirus-based vectors provide a versatile cancer immunotherapy platform, enabling the expression of immunostimulatory molecules and cancer-specific antigens. While infections with pathogenic viruses are well known to modulate extracellular vesicle (EV) biogenesis and function, the extent to which therapeutic poxviral vectors influence EV secretion by immune cells and thereby affect therapeutic efficacy remains underexplored. In this study, we showed that poxviruses, including the clinically relevant Modified Vaccinia Ankara (MVA), stimulate the secretion of small EVs (sEVs) containing viral proteins and immune-related signatures from peripheral blood mononuclear cells (PBMCs). Using an engineered MVA vector, we demonstrated the transfer of virus-encoded therapeutic payloads to sEVs, including the model ovalbumin (OVA)-derived peptide SIINFEKL presented by the class I major histocompatibility complex (MHC I) and the immune activators interleukin-12 (IL-12) and CD40 ligand (CD40L). Depending on the isolation method, these sEVs stimulated SIINFEKL-specific CD8 T cells with varying efficiencies in vitro. Remarkably, intravenous injection of these sEVs, but also of the soluble secretome from the same cells, into E.G7-OVA lymphoma-bearing mice reduced tumor growth to an extent comparable to the virus itself. Taken together, our findings indicate that EVs released from immune cells infected with engineered therapeutic poxviruses exert potent antitumor activity. These vesicles represent actionable mediators whose secretion and functionalization can be harnessed to improve viral vector-based immunotherapies, as well as being considered as therapeutic vectors in their own. - Source: PubMed
Walther LucasMittelheisser VincentClaudepierre Marie-ChristineBochler LouisRompais MagaliDeforges JulesSilvestre NathalieLarnicol AnnabelCarapito ChristineQuémeneur EricGoetz Jacky GRittner KarolaHyenne Vincent - Inflammatory bowel disease (IBD) is consistently associated with an increased risk of venous thromboembolism, particularly during active disease and hospitalization, yet thrombosis in this context extends beyond a transient inflammatory complication. Emerging evidence supports a unifying thromboinflammatory framework in which chronic intestinal inflammation promotes systemic vascular activation. Endothelial dysfunction represents a central interface in this process and is characterized by reduced nitric oxide bioavailability, increased expression of adhesion molecules, angiogenic remodeling, and glycocalyx disruption, collectively shifting the vascular surface toward a proadhesive and procoagulant phenotype. In parallel, dysregulation of coagulation pathways sustains thrombin generation through enhanced tissue factor signaling, elevated procoagulant factors, most consistently factor VIII, impaired endogenous anticoagulant mechanisms including the protein C and antithrombin systems, and features of hypofibrinolysis. Platelet activation further amplifies these disturbances via CD40 ligand (CD40L)-mediated endothelial crosstalk, platelet leukocyte aggregate formation, and imbalance of the von Willebrand factor (VWF)-ADAMTS13 axis, reinforcing a self perpetuating loop between inflammation and coagulation. Although mechanistic plausibility is strong and multiple biomarkers of endothelial and hemostatic activation have been described, much of the current evidence derives from cross sectional or associative studies, with limited prospective validation linking individual pathways to incident thrombotic outcomes in IBD specific cohorts. Taken together, thrombosis in IBD reflects sustained systemic thromboinflammatory dysregulation rather than an isolated complication of flares. Future longitudinal studies integrating vascular biomarkers with adjudicated thrombotic events are essential to refine risk stratification and inform individualized thromboprophylaxis strategies. - Source: PubMed
Publication date: 2026/06/16
Šantić RokoPavlović NikolaKumrić MarkoVilović MarinoBožić Joško - The CD40-CD154 costimulatory axis serves as a central hub bridging innate and adaptive immunity, regulating antigen presentation, T-cell priming, B-cell activation, germinal center formation, and antibody class switching. In transplantation, this pathway drives donor-reactive T-cell expansion, dendritic cell (DC) licensing, and donor-specific antibody generation, contributing to both acute and chronic allograft rejection. Recent discoveries have expanded the classical linear model into a multidimensional signaling network. This network encompasses canonical CD40-TNF receptor-associated factor (TRAF)-NF-κB signaling, CD154 reverse signaling, and alternative receptor engagement-particularly through integrins such as CD11b. These insights explain the differential efficacy of CD154 versus CD40 blockade and inform next-generation therapeutic design. Concurrently, renewed clinical interest has emerged following the development of fragment crystallizable (Fc)-engineered anti-CD154 antibodies that circumvent first-generation thromboembolic toxicity. Here, we synthesize current understanding of CD40-CD154 molecular architecture, upstream triggers, downstream signaling networks, crosstalk with other immune pathways, and cell type-specific outputs. We evaluate therapeutic candidates in clinical development, discuss unresolved questions regarding long-term safety and biomarker development, and highlight future directions including cell-targeted intervention and tolerance-inducing combination strategies. - Source: PubMed
Publication date: 2026/05/28
Wang KunxiongLi TaoYan TingHara HidetakaWang Yi