CD80
- Known as:
- CD80
- Catalog number:
- 11-287-C025
- Product Quantity:
- 0.025 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD80
Related genes to: CD80
- 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: CD80
Activation B7-1 antigen,B7,B7,Cd80,Mouse,Mus musculus,T-lymphocyte activation antigen CD80Activation B7-1 antigen,B7,BB1,CD28LG,CD28LG1,CD80,CTLA-4 counter-receptor B7.1,Homo sapiens,Human,LAB7,T-lymphocyte activation antigen CD80Activation B7-1 antigen,CD80,Oryctolagus cuniculus,Rabbit,T-lymphocyte activation antigen CD80anti-CD80anti-CD80anti-CD80anti-CD80anti-CD80anti-CD80 (1G1)anti-CD80 (3D7)anti-CD80 (3E10)anti-CD80 (4A4)anti-CD80 (1G1)anti-CD80 (1G1) type: Primary antibodies host: Mouseanti-CD80 (2A2) Related articles to: CD80
- Traumatic brain injury (TBI) induces a sustained neuroinflammatory response involving activated microglia and infiltrating myeloid cells, contributing to secondary brain damage and long-term neurological dysfunction. Modulating these inflammatory responses toward a more reparative phenotype represents a promising therapeutic strategy, but achieving targeted delivery within the injured brain remains a major challenge. Here, we developed a targeted, non-viral gene-editing platform using lipid nanoparticles (LNPs) encapsulating CRISPR-Cas12a components directed against MAPK9, a key mediator of inflammatory signaling. LNPs were functionalized with an Iba-1 antibody to enhance targeting of Iba-1 + myeloid cells following intranasal administration. In primary bone marrow-derived macrophages and primary microglia, CRISPR-mediated MAPK9 targeting reduced MAPK9 expression and suppressed pro-inflammatory activation, decreasing iNOS, NLRP3, CD80, and CCL2 while increasing the anti-inflammatory/reparative markers CD206 and Arg1. In a mouse model of TBI, intranasally delivered Iba-1-targeted CRISPR-LNPs showed preferential association with Iba-1 + cells compared with NeuN+ neurons in the injured cortex and reduced MAPK9 expression within Iba-1 + cells. CRISPR-LNP treatment attenuated microglial/macrophage activation, reduced pro-inflammatory cytokine expression, and decreased iNOS+/Iba-1 + cells while increasing CD206+/Iba-1 + cells in the peri-contusional cortex, supporting a shift toward a less inflammatory phenotype. Treatment also exhibited a favorable safety profile, with no detectable toxicity in the major organs examined. Together, these findings demonstrate that intranasal delivery of Iba-1-targeted CRISPR-LNPs enables effective MAPK9 modulation in Iba-1 + myeloid cells within the injured brain and attenuates acute neuroinflammation following TBI. This non-invasive therapeutic platform provides a promising approach for targeted modulation of neuroinflammatory responses after brain injury. - Source: PubMed
Publication date: 2026/08/27
Kara GoknurHolcomb MorganHijazi Asmaa AAli YaqoobLópez-Espinosa JessicaCruz-Pineda LeonardoPark PeterFlinn HannahTaylor NoahGalbraith TylerMcMahon LornaRostomily RobertLeonard FransiscaVillapol Sonia - Regenerative endodontic therapy aims to restore the pulp-dentin complex through biological approaches; however, current cell-free techniques often fail to achieve true dental pulp regeneration and may result in fibrous tissue formation or canal calcification. This study investigated dynamic hydrogels as advanced scaffolds for dental pulp stem cell (DPSC)-mediated regeneration, leveraging their viscoelastic properties to regulate cellular behavior and immune responses. - Source: PubMed
Publication date: 2026/08/12
AlMaimouni YaraYuan WeihaoHoutari ShorouqMoshaverinia Alireza - Ocular diseases, such as neovascular age-related macular degeneration (nAMD) and proliferative vitreoretinopathy (PVR), have a fibrotic component that negatively impacts vision. Unfortunately, few treatments are available to mitigate fibrosis in the eye. The clearance of inflammatory cells proceeds, at least in part, through the intrinsic cell death pathway in which Bcl-2 family members play integral roles. Here, we assessed the influence of Bcl-2 expression in mononuclear phagocytes (MP) on the engagement and clearance of inflammatory cells, choroidal neovascularization (CNV), and subsequent subretinal fibrosis in a mouse laser-induced CNV model. Lack of Bcl-2 expression in MP (Bcl-2 mice) decreased neutrophil (Gr1) and microglia (Iba1) presence without impacting M1 (CD80) and M2 (CD206) macrophage presence, CNV, or fibrosis during the first 2 weeks following laser photocoagulation. Later, after inflammation dampens, decreased later-stage fibrosis and CNV were noted in Bcl-2 mice, which were accompanied by increased presence of M2 macrophages (CD206). However, how these increased levels of CD206 M2 macrophages in the absence of Bcl-2 contribute to decreased CNV and fibrosis remains unknown. To address whether Bcl-2 expression affects other forms of ocular fibrosis, we utilized the dispase PVR model. Bcl-2 mice, or treatment of wild-type mice with Bcl-2 inhibitors, significantly decreased fibrosis in the PVR model. Furthermore, Bcl-2 inhibitors mitigated CNV and fibrosis (collagen I-defined) in wild-type mice during laser photocoagulation. Thus, inhibition of Bcl-2 activity prevents the late-stage clearance of CD206 M2 macrophages during nAMD and PVR, mitigating ocular neovascularization and fibrosis. - Source: PubMed
Publication date: 2026/08/20
Song Yong-SeokWang ShoujianDarjatmoko Soesiawati RSheibani NaderSorenson Christine M - Natural Killer (NK) cell-mediated immunosurveillance is a cornerstone of anti-tumor defense, yet its efficacy can be compromised by common clinical medications. Paracetamol (APAP) and metformin (MET) are widely used for pain and metabolic management in cancer patients, but their unintended effects on the immune-tumor interface remain poorly understood. MCF-7 breast cancer cells (Luminal A subtype) were treated with APAP or MET and co-cultured with primary expanded NK cells (CD3CD56CD16). We evaluated cell proliferation, cell cycle distribution, and the enrichment of the CD44CD24 cancer stem-like cell (CSC-like) subpopulation. Transcriptional changes in immune checkpoints (), stress ligands (), and costimulatory molecules were quantified via RT-qPCR. Despite inhibiting MCF-7 growth (IC at 48 h: 11.86 mM for APAP; 21.11 mM for MET), both drugs induced a "therapeutic paradox" by promoting an immune-evasive phenotype. APAP and MET significantly enriched the CD44CD24 CSC-like subpopulation to 75.31% and 68.31%, respectively, compared to 11.00% in controls. Molecular analysis revealed a robust upregulation of (19.9-fold by APAP) and (16.4-fold by MET), alongside increased and transcription. Consequently, drug-treated cells exhibited marked resistance to NK-mediated apoptosis and necrosis. NK cells preferentially eliminated non-stem cells (non-CSCs), inadvertently further concentrating the highly resistant CSC-like subpopulation. Additional experiments revealed that APAP directly impaired NK-cell survival and reduced the proportion of CD3CD56 cells, whereas MET exerted minimal effects on NK cells, suggesting distinct mechanisms underlying the observed reduction in NK-mediated cytotoxicity. Under the experimental conditions employed in this study, APAP and MET were associated with reduced susceptibility of MCF-7 cells to NK-mediated killing through distinct but partially overlapping mechanisms, including CSC-like enrichment and transcriptional activation of immune-evasion pathways. Although these findings were obtained in a mechanistic in vitro model using supra-physiological drug concentrations, they identify potential mechanisms that warrant further validation in physiologically relevant experimental systems and in vivo models. - Source: PubMed
Publication date: 2026/08/12
Truong Nhat ChauHuynh Nhi ThaoTrinh Khanh GiaPhan Anh Thuy-KieuLe Duyen Thi-ThuyPham Phuc Van - Flow-cytometric readouts in acute myeloid leukemia (AML) may depend on specimen source and processing. We assessed whether sample source (peripheral blood [PB] vs. bone marrow [BM]) and cryopreservation influence immune-evasion-related markers on AML blasts. Paired PB and BM samples from 19 adults were analyzed fresh and after cryopreservation. Viable CD45 singlets were assessed for ULBP1-6, MICA/B, CD34, CD44, CD70, CD80, and CD184 using median fluorescence intensity (MFI) and relative fluorescence index (RFI). Paired comparisons used two-sided Wilcoxon signed-rank tests with Benjamini-Hochberg correction across six markers within each endpoint and comparison. Discordance was also assessed using a predefined conventional 20% reference threshold. After adjustment, RFI did not differ between fresh and cryopreserved samples within PB or BM, or between fresh PB and BM. In cryopreserved samples, PB and BM differed for CD70 (q = 0.042) and ULBP1-6 (q = 0.028). Cryopreservation increased MFI for CD184 and ULBP1-6 in PB and BM and for MICA/B in PB; no PB-BM MFI difference remained significant. Threshold-based classification was discordant for CD34, CD44, CD80, CD184, MICA/B, and ULBP1-6 in 5.3-38.9% of pairs, whereas CD70 showed none. Cohort-level differences were limited to specific markers and conditions, while patient-level threshold discordance persisted. Sample source and cryopreservation should therefore be considered when interpreting threshold-based classifications. - Source: PubMed
Publication date: 2026/08/09
Richter SvenLeinauer BenediktThoma AliciaSchmälter Ann-KristinWaidhauser JohannaSchmid ChristophRank AndreasLöhr Phillip