CD40LG Antibody
- Known as:
- CD40LG Antibody
- Catalog number:
- abx000686
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- CD40LG Antibody
Related genes to: CD40LG Antibody
- 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: CD40LG Antibody
Related articles to: CD40LG Antibody
- Whole blood transfusion is increasingly used in trauma resuscitation. However, stored whole blood units demonstrate increasing susceptibility to tissue plasminogen activator-mediated fibrinolysis despite paradoxical increases seen in plasminogen activator inhibitor-1 (PAI-1) activity over time. Whether early variability in PAI-1activity exists across whole blood units and the biologic contributors to this variability remain unclear. Two distinct donor pools were identified: one with high PAI-1 activity and one with low PAI-1 activity. We set out to determine whether PAI-1 activity in whole blood donors primarily comes from the endothelium or from platelet degranulation. - Source: PubMed
Publication date: 2026/04/23
Maginot Elizabeth RBarmettler Nicolle KGawargi Flobater IMoore Ernest EWhite Collin MHiser Dylan CClegg Ashley ASextro Kyle SMoody Trace BVolk Grace EMoore Hunter BGoodman NatashaBobr AlehHenry ReynoldBarrett Christopher D - The bidirectional interaction between inflammation and thrombus formation plays an important role in myocardial infarction (MI) with IL (interleukin)-6 as a central mediator. If anti-inflammatory therapy modulates coagulation factors, and platelet activation in patients with MI is not clear. - Source: PubMed
Publication date: 2026/04/23
Ueland ThorDahl Tuva BMichelsen AnnikaKleveland OlaAndersen Geir ØysteinAnstensrud Anne KristinHuse CamillaWoxholt SindreBroch KasparGullestad LarsLibby PeterAukrust PålHalvorsen Bente - IL-10-producing B cells exert immunosuppressive effects, yet their low abundance and poor in vitro viability have limited their therapeutic application. Here, we developed a stromal coculture system using MS5 cells engineered to express human CD40L, BAFF, and IFN-β1 (MS5-3F, for "3 factors"), which enables robust induction and greater than 1000-fold expansion of human IL-10-producing B cells. The expanded cells showed phenotypic and transcriptional profiles characteristic of unswitched (IgM+) plasmablasts and potently suppressed CD4+ T cell proliferation in an IL-10-dependent manner. MS5-3F-expanded B cells also increased the frequency of regulatory T cells in vitro, an effect that was not abrogated by IL-10/IL-10R blockade, suggesting contributions from additional mechanisms. IL-10 production originated predominantly from naive B cells, rather than memory B cells. Furthermore, B cells from patients with systemic lupus erythematosus, despite impaired IL-10 production under conventional conditions, were efficiently differentiated into IL-10-producing B cells using this system. The expanded cells showed minimal IgG-secreting output. Our platform offers a scalable strategy for generating human regulatory B cells, laying the foundation for B cell-based immunotherapies. - Source: PubMed
Publication date: 2026/04/22
Kawakami RyoImabayashi KeisukeBaba AkemiSaito YuichiKawata KazuhikoYada YutaroShibata AiriIto RinkaKurasawa RyoHiguchi RyotaPark SungyeonNiiro HiroakiTanaka ShinyaBaba Yoshihiro - - Source: PubMed
Publication date: 2026/04/21
Alroqi FayhanAlJaber Abdulrahman NAlthubaiti NoufAl Tuwaijri AbeerAlzaaqi ShouqBarhoumi TliliAlmutairi AbduarahmanAlmuzzaini BaderAlsayegh LeenaNogoud MaysaAljedaie Modhi - Extracorporeal membrane oxygenation (ECMO) can trigger a systemic inflammatory response syndrome (SIRS) with activation of inflammatory, endothelial, and coagulation system pathways. We assessed in a randomized trial whether a) sweep flow nitric oxide (sNO) reduces these responses, b) what the temporal trajectory of these markers post-ECMO commencement is, and c) how serum marker concentrations are associated with survival. Fifty-three patients were randomized (25 sNO, 28 control). Serum levels of inflammatory cytokines (IL-1, IL-6, IL-8, IL-10, TNF-α), complement (C1q, C3, C4, C5a, C9, factor H, factor B), immune regulators (CD40L, P-Selectin), and coagulation factors (PF4, MBL, ADAMTS13) were measured at (t0) and 1, 12, 24 hours post (t1-t3) ECMO initiation. Sweep flow nitric oxide did not alter serum biomarker trajectories. Across sNO and control groups, serum marker concentrations declined from t0 to t1 with variable patterns thereafter, but no consistent ECMO-associated elevation. Elevated IL-6 and IL-8 before and after ECMO commencement were associated with mortality, whereas higher P-Selectin, CD40 Ligand, and PF4 correlated with survival. Sweep flow nitric oxide did not modify markers of inflammation, endothelial, or coagulation activation during ECMO. Evidence of an ECMO-induced cytokine storm was absent, but serum biomarkers predicted mortality in ECMO-supported neonates and children. - Source: PubMed
Publication date: 2026/04/17
Mattke Adrian CSchlapbach Luregn JTakashima MariJohnson Kerry EMcPherson StephenVenugopal Prem SBlumenthal Antje