Human Polyclonal CD40LG Ab
- Known as:
- Human Polyclonal CD40LG Antibody
- Catalog number:
- a0327
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal CD40LG
Related genes to: Human Polyclonal CD40LG Ab
- 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 Polyclonal CD40LG Ab
Related articles to: Human Polyclonal CD40LG Ab
- Peripheral-blood transcriptomic profiling can capture molecular heterogeneity in systemic lupus erythematosus (SLE), but discovery-stage signatures often show limited transportability across cohorts and validation layers. This study aimed to establish a staged whole-blood transcriptomic framework and to derive a compact, biologically interpretable activity score. - Source: PubMed
Publication date: 2026/06/06
Zhang ChuanweiPang LijunZhu ZihengWang JianingHuang Chuanbing - T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subtype of ALL characterized by unfavorable clinical outcomes. Despite significant progress in deciphering the genetic and epigenetic landscapes of T-ALL, the underlying molecular mechanisms, particularly in non-early T-cell precursor (non-ETP) T-ALL, remain incompletely understood. In this study, functional assays were performed using three well-characterized non-ETP T-ALL cell lines. In vivo therapeutic efficacy was evaluated using non-ETP T-ALL xenograft models. Transcriptomic profiling was performed by RNA sequencing (RNA-seq) followed by bioinformatic analysis. Publicly available clinical datasets from T-ALL patients were mined to analyze survival outcomes. We found that activation of CD40 ligand (CD40LG) or CD28 accelerates cell-cycle progression and enhances the migratory capacity of non-ETP T-ALL cells, with CD40LG uniquely upregulating CXCR4 to mediate bone marrow tropism. Further RNA-seq and functional validation identified Rho GTPase signaling, specifically RhoA/Rac1/Rac2, as a pivotal downstream effector of CD40LG/CD28, leading to therapeutic resistance to PI3K inhibition. Pharmacological blocking RhoA or Rac1 using small-molecule compounds not only induces remarkable cytotoxicity but also sensitizes resistant cells to PI3K inhibitors, both in vitro and in vivo. Clinically, elevated expression of , , , or correlates with poor prognosis in non-ETP T-ALL patients. These findings uncover a novel CD40LG/CD28-Rho GTPase axis as a key driver of pathogenesis and a potential therapeutic vulnerability in non-ETP T-ALL, providing a new target for precision intervention and a promising strategy to overcome therapeutic resistance. - Source: PubMed
Publication date: 2026/06/11
Yang YanLu WeiZhu ZhexiLi ChenyangGuo ZihaoZhang Han - : Acute pulmonary embolism (PE) and hospitalization-requiring community-acquired pneumonia (CAP) may present with overlapping clinical, laboratory, and radiological features. Soluble CD40 ligand (sCD40L) is a platelet-derived thrombo-inflammatory mediator that may be influenced by both thrombotic and inflammatory processes. This study retrospectively compared on-admission serum sCD40L concentrations between selected hospitalized patients with established acute PE and selected patients with hospitalization-requiring CAP. : This single-center retrospective exploratory comparative biomarker study included 82 hospitalized adults: 48 with computed tomography pulmonary angiography (CTPA)-confirmed acute PE and 34 with hospitalization-requiring CAP defined using CURB-65-supported admission criteria. Stored admission serum samples were used for sCD40L measurement. Between-group comparison was the primary analysis; receiver operating characteristic (ROC) analysis was performed as a secondary exploratory description of the apparent within-sample discriminatory signal. : sCD40L was higher in acute PE than in hospitalization-requiring CAP (median 821.3 vs. 629.0 pg/mL; < 0.001). ROC analysis demonstrated a strong exploratory within-sample discriminatory signal (AUC 0.951, 95% CI 0.905-0.997). After excluding five patients with recorded antiplatelet or rivaroxaban exposure, the apparent signal remained similar (AUC 0.945; bootstrap 95% CI 0.891-0.984), and sCD40L remained associated with PE in a Firth-penalized model adjusted for platelet count and COPD (OR 3.39 per 50 pg/mL, 95% CI 2.00-7.71; < 0.001). : In this retrospective selected two-group comparison, on-admission serum sCD40L concentrations were higher in established acute PE than in hospitalization-requiring CAP. ROC-derived estimates should be interpreted only as apparent within-sample discrimination and not as a replacement for D-dimer, clinical probability assessment, or imaging-based PE diagnosis. Prospective validation in unselected suspected-PE cohorts is required before any diagnostic or clinical use can be considered. - Source: PubMed
Publication date: 2026/06/16
Çelik OnurKılıç Adil FurkanKuralay YunusAfşin Dursun Erol - Due to its central role in regulating adaptive immune responses through CD40 engagement, the CD40 ligand (CD40L) represents an attractive therapeutic target for inflammatory and autoimmune diseases. Here, CD40L-specific affibody molecules were generated by directed evolution using an Escherichia coli surface display platform. Two affibody candidates were identified that specifically recognized human CD40L on the surface of activated primary T cells. To exploit the homotrimeric architecture of CD40L, the affibody candidates were genetically fused to the NC1 domains of human collagen XV or XVIII, yielding well-defined homotrimeric constructs. The trimeric affibody formats were characterized with respect to oligomeric state, thermal stability, binding kinetics, cellular target engagement, and functional inhibition of CD40 signaling. NC1-mediated trimerization resulted in an approximately 100-fold improvement in apparent affinity, markedly enhanced binding to membrane-bound CD40L, and potent inhibition of CD40L-induced NF-κB activation in a reporter cell assay. Collectively, these results establish collagen XV and XVIII NC1 domains as effective trimerization modules for affibody molecules and highlight a strategy for engineering Fc-independent, multivalent antagonists targeting CD40L. - Source: PubMed
Publication date: 2026/06/24
Westerberg CorneliaSorini ChiaraAl-Haddad MariamMehari HannaStåhl StefanJagodic MajaLöfblom John - 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