Mouse B7-1 CD80 ELISA kit
- Known as:
- Mouse B7-1 CD80 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- LF-EK50715
- Product Quantity:
- 1
- Category:
- Elisa Kits
- Supplier:
- Abfron
- Gene target:
- Mouse B7-1 CD80 ELISA kit
Related genes to: Mouse B7-1 CD80 ELISA kit
- Gene:
- CD80 NIH gene
- Name:
- CD80 molecule
- Previous symbol:
- CD28LG, CD28LG1
- Synonyms:
- B7.1, B7-1
- Chromosome:
- 3q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-14
- Date modifiied:
- 2016-10-05
Related products to: Mouse B7-1 CD80 ELISA kit
Related articles to: Mouse B7-1 CD80 ELISA kit
- Circulating myeloid cells are critical regulators of pancreatic ductal adenocarcinoma (PDAC) progression. However, their postoperative dynamics and clinical relevance remain poorly defined. In a prospective longitudinal study, blood was collected from PDAC patients prior to surgery and on postoperative day 7. Flow cytometry was used to characterize monocytes, including classical (CM), intermediate (IMM), and non-classical (NCM) subsets, along with regulatory and co-stimulatory molecules (CD71, CD40, CD141, CD80, CD86, PD-L1). Cytokine levels (IL-6, IL-10, TNF-α, IL-1β) were quantified by ELISA and correlated with clinical parameters and survival. Total monocytes and CM increased significantly at day 7, whereas IMM and NCM decreased. CD71, CD141, CD80, and CD86 expression were significantly altered across subsets, with the most pronounced reduction observed in CD86 expressing NCM. CD86 expressing NCM correlated inversely with systemic bilirubin but not CEA, lymphocytes, thrombocytes, or hospital stay. IL-6 and IL-10 increased postoperatively; IL-10 showed a tendency toward inverse correlation with CD86 NCM. Low CD86 expression on NCM at day 7 was associated with reduced survival and higher relapse probability. CD86 expression on NCMs is profoundly reduced after PDAC surgery and serves as a prognostic biomarker linked to inflammation, bilirubin metabolism, survival, and recurrence. Postoperative monocyte profiling may improve risk stratification and inform early clinical decision-making. - Source: PubMed
Publication date: 2026/06/01
Arnold Lisa-SophieJacobsen AnneKuchenreuther IsabelleMazurie JohanneClausen Finn NiklasLitau MelanieKlöckner SebastianCzubayko FranziskaBancke Laverde Bruno LeonardoAmin YazanWeisel NadineKlösch BettinaMerkel SusanneBrunner MaximilianKrautz ChristianGrützmann RobertMittelstädt AnkeWeber Georg FDavid Paul - Inflammatory response associated with Apical Periodontitis (AP) is shaped by neuroimmune signaling mediated by neuropeptides and cytokines that regulate interactions among sensory neurons, immune cells, and stromal cells in the periapical microenvironment. To investigate these mechanisms, this study employed an in vitro multicellular culture system modeling key neuroimmune features relevant to AP rather than anatomical lesion formation. Neuron-like cells (NLCs) were generated from periodontal ligament cells (PDLCs) using dual-SMAD inhibition, and bi-directional paracrine and juxtacrine signaling between NLCs, PDLCs, and THP-1-derived macrophages (MQs) was examined under lipopolysaccharide (LPS)-induced inflammatory conditions. Neuropeptides released by NLCs, Substance P (SP) and Calcitonin Gene-Related Peptide (CGRP), enhanced LPS-driven inflammatory responses in PDLC-MQ paracrine systems, characterized by increased macrophage expression of CD68 and CD80 and elevated secretion of IL-1β and TGF-β1. In contrast, during PDLC-MQ juxtacrine interactions, NLC-derived neuropeptides supported a regulatory profile, with reduced expression of CD68, CD80, and STAT1 and decreased production of TNF-α and IL-1β. Reciprocally, conditioned media from LPS-treated PDLC-MQ co-cultures modulated NLC signaling by increasing TRPV1 expression, while IL-10 present in the conditioned media suppressed TRPA1 expression, resulting in an overall CGRP-dominant and SP-suppressed neuropeptide profile. These findings identify a dynamic, bi-directional neuroimmune circuitry among neuron-like cells, macrophages, and periodontal ligament cells that differentially regulates inflammatory and regulatory signaling in a system relevant to Apical Periodontitis, providing mechanistic insight into neuroimmune coordination during periapical inflammation. - Source: PubMed
Publication date: 2026/06/11
Menon NanditaMayorova Tatiana DSenatore AdrianoKishen Anil - 2,4-Dichlorophenoxyacetic acid (2,4-D) is a widely used herbicide, yet its immunomodulatory properties remain insufficiently characterized, raising concerns about potential adverse outcomes. This study examined whether 2,4-D, at environmentally and biologically relevant concentrations, influences inflammatory responses in RAW 264.7 macrophages under basal and lipopolysaccharide (LPS)-stimulated conditions. Under basal conditions, 2,4-D had no effect on inflammatory mediator production or activation of nuclear factor-kappa B (NF-κB) p65, extracellular signal-regulated kinase (ERK1/2), or p38 signaling pathways. However, 2,4-D markedly potentiated LPS-induced responses, increasing pro-inflammatory cytokines (IL-6, TNF-α, and IL-1β), COX-2 expression, nitric oxide production, and CD80 surface expression without cytotoxicity. Consistently, 2,4-D enhanced LPS-induced activation of NF-κB p65, ERK1/2, and p38 pathways. Comparative Toxicogenomics Database analysis revealed 167 overlapping genes associated with both 2,4-D and LPS exposure. Integrative pathway, PPI, and Metascape analyses identified RELA (NF-κB p65) and MAPK1 (ERK2) as key mediators. Pharmacological inhibition confirmed that IL-6 and COX-2 responses depended mainly on NF-κB p65 and ERK1/2, whereas CD80 up-regulation was predominantly NF-κB p65 dependent. Collectively, these findings provide new mechanistic insight into the amplification of macrophage inflammatory responses by 2,4-D under immune-challenged conditions via NF-κB p65 and ERK1/2 signaling pathways. - Source: PubMed
Publication date: 2026/06/11
Kanitwithayanun JantamasChujan SuthipongBabar Nedsai UddinRittapai NoppawanVajeethaveesin NutsiraSatayavivad Jutamaad - Chemodynamic therapy (CDT) is severely limited by insufficient reactive oxygen species (ROS) generation and high glutathione (GSH)-mediated antioxidant defense in the tumor microenvironment. To address these challenges, we developed an ultrasound-triggered self-assembled cascade nanozyme (HSA-GOx-CuO) that amplifies ROS production through triple synergy: glucose oxidase (GOx)-mediated glucose depletion (starvation therapy) and hydrogen peroxide self-supply, CuO-driven GSH depletion, and synergistic CDT. In vitro studies using 4T1 breast cancer cells showed that under US stimulation, HSA-GOx-CuO significantly elevated intracellular ROS levels, induced potent apoptosis (late apoptotic rate: 85.1%), and promoted dendritic cell maturation (97.9% CD80CD86 DCs). In vivo, the nanozyme efficiently accumulated in tumors via the enhanced permeability and retention effect, achieving a 92.6% tumor inhibition rate with strong growth suppression. This US-activatable cascade nanoplatform integrates starvation therapy and GSH depletion, offering a safe and novel strategy for precision synergistic CDT of tumors. - Source: PubMed
Publication date: 2026/06/08
Zhao ZiweiLi LiangyuQi WenjingZhou YijunLu MinLuo Yong - Targeting protein-protein interactions (PPIs) with small molecules is historically challenging due to shallow, solvent-exposed interfaces that lack classical binding pockets. Furthermore, employing traditional structure-based virtual screening (SBVS) across ultralarge chemical spaces to find novel chemotypes imposes prohibitive computational bottlenecks. Here, we report the first prospective, real-world application of the PyRMD2Dock platform, an AI-enforced SBVS workflow that integrates machine learning and standard docking available within the PyRMD Studio suite. To target the structurally demanding immune receptor CD28, a chemically diverse subset of 2.4 million molecules from the Enamine REAL Diversity Space was docked into a cleft adjacent to the canonical ligand interface. These data were used to train 672 classification models, and the optimized model rapidly screened the remaining ∼46 million compounds. Following interaction filtering and clustering, 232 highly prioritized ligands were identified. Experimental validation of 150 purchased candidates yielded a strong hit rate, identifying multiple direct CD28 binders. Lead compounds and exhibited submicromolar affinity ( = 343.8 nM and 407.1 nM, respectively), potent CD28-CD80 disruption, and functional blockade in cellular reporter assays. Furthermore, these compounds successfully reduced cytokine secretion in primary human tumor-PBMC and epithelial tissue coculture models. This study validates PyRMD2Dock as a highly scalable, effective protocol for mining massive chemical libraries to discover small-molecule modulators of challenging immune receptor interfaces. - Source: PubMed
Publication date: 2026/06/11
Upadhyay SaurabhRoggia MicheleYuan ShaorenCosconati SandroGabr Moustafa T