CD80
- Known as:
- CD80
- Catalog number:
- 1F-287-T100
- Product Quantity:
- 100 tests
- 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
- Pulmonary fibrosis is a progressive disease marked by excessive fibrotic transformation of lung tissue. Paricalcitol, a selective vitamin D receptor (VDR) agonist, has shown promise in reducing fibrosis in experimental models, primarily due to its anti-inflammatory and anti-fibrotic properties. This study evaluates the therapeutic effects of paricalcitol on bleomycin-induced pulmonary fibrosis in a rat model. - Source: PubMed
Kriventsov Maxim AEnzel Darya ASataieva Tatyana P - Sepsis seldom presents as a uniform immune phenotype. Inflammation and immune suppression often overlap, but their balance shifts across patients, organs, and illness stages. Macrophages sit within this variation, coordinating cytokine output, microbial clearance, antigen processing, and presentation. Lipophagy removes lipid droplets through selective autophagy. The released fatty acids can feed mitochondrial β-oxidation, helping macrophages balance lipid storage with energy demand. Reduced flux may instead leave excess droplets, compromise mitochondrial function, and blunt antimicrobial activity. Whether this sequence directly drives sepsis-associated immunoparalysis remains uncertain. Protein S-palmitoylation offers a second potential control point through reversible cysteine S-acylation. Studies have linked this modification to ATG16L1 and ATG4B, and to immune regulators including MYD88, NLRP3, and CD80. Most of that evidence, however, comes from models other than sepsis, so its relevance cannot be assumed. This review therefore examines the proposed links among macrophage lipophagy, immunometabolic failure, and sepsis-associated immunoparalysis while keeping experimentally established observations separate from mechanistic inference. Taken together, current findings support S-palmitoylation as a plausible regulatory layer, but they do not establish an integrated causal axis linking S-palmitoylation, lipophagy, and immunometabolism in sepsis. This framework awaits direct testing in primary macrophages, organ-specific sepsis models, and longitudinal clinical cohorts. - Source: PubMed
Publication date: 2026/09/20
Wang YisenZhang LiangZhang LiyaoJiang HongkunCao Meiling - The generation and maintenance of effective tumor-specific CTL responses require more than antigen recognition. In most settings, TCR engagement must be accompanied by co-stimulatory input, with the B7-1/B7-2-CD28 axis being one of the best-characterized examples. When this second signal is weak or absent, tumor-reactive CD8+ T cells may recognize tumor antigens but fail to expand, survive, or acquire and sustain cytotoxic activity. Tumors take advantage of this vulnerability by reducing co-stimulatory ligand availability, increasing inhibitory checkpoint signaling, and remodeling the tumor microenvironment in ways that further restrict T-cell activation. Depending on the stage and context of dysfunction, this shift may favor anergy-like dysfunction, impaired persistence and apoptotic attrition, or, under persistent antigen exposure and sustained inhibitory signaling, exhaustion-associated dysfunction, thereby promoting immune escape. This review examines how reduced or functionally restricted B7-CD28 co-stimulation impairs CTL activation, intratumoral reactivation, and persistence, and how checkpoint signaling, suppressive immune cells, metabolic stress, and stromal barriers compound this defect within tumors. We also evaluate strategies intended to restore or bypass inadequate co-stimulatory input, distinguishing established checkpoint-based interventions from co-stimulatory agonists, engineered T-cell therapies, multispecific antibodies, and gene-based approaches that remain preclinical or early translational in many settings. We propose that mechanism-matched therapy should be guided by the phase at which the dominant barrier arises-tumor-reactive CD8+ T-cell priming, intratumoral CTL reactivation, or long-term CTL persistence. - Source: PubMed
Publication date: 2026/07/28
Ma JunjieChen JingMiao TianrunLi YehongLi YongmengZhao LeiTian Hui - As a prevalent malignancy, liver cancer ranks as the third most common cause of cancer mortality globally. Within the tumor microenvironment, tumor-associated macrophages (TAMs) exhibit contrasting functional phenotypes: the anti-tumor M1 type and the pro-tumor M2 type. Reprogramming TAMs from the M2 to the M1 phenotype has emerged as a promising immunotherapeutic strategy. Here, we engineered a multi-nano therapeutic system, PAH@HMMDN@R848, by loading a TLR7/8 agonist (R848) onto hollow MnO2 nanoparticles (HMMDN) and coating with polyallylamine hydrochloride (PAH). In vitro, this system efficiently repolarized M2 macrophages to the M1 phenotype, evidenced by decreased CD206, Arg-1, IL-10 and increased CD80, iNOS, TNF-α (P < 0.05). Under acidic/glutathione-rich conditions, HMMDN degraded to release Mn2+, which served as a T1-weighted MRI contrast agent with a high relaxivity (r1 = 5.255 mM-1 s -1). Mechanistically, PAH@HMMDN@R848 activated both NF-κB (via R848) and STING (via Mn2+) pathways, leading to synergistic M1 polarization. In a subcutaneous H22 liver cancer mouse model, intratumoral injection of PAH@HMMDN@R848 significantly suppressed tumor growth (tumor inhibition rate 80.6%) without obvious systemic toxicity. Immunohistochemistry and cytokine analysis revealed that the treatment increased M1 macrophage infiltration (CD80+) and reduced M2 macrophages (CD206+) within tumors, along with elevated TNF-α/iNOS and decreased IL-10/Arg-1. This study presents a multifunctional nanoplatform capable of TAMs reprogramming and MRI diagnosis, offering a promising approach for liver cancer theranostics. - Source: PubMed
Publication date: 2026/09/18
He Pei-PeiHou Zheng-JuLi Han-MeiZhang Ji-XuanChen An-QiMiao Quan-YouYang Chao-FengYu Jin-HongLi Yang - Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the selective loss of motor neurons in the brain and spinal cord with evidence of local neuroinflammation. Regulatory T cells (Treg) exert neuroprotective effects and correlate with disease progression, but central mechanisms governing Treg development during ALS remain unclear. We investigated the thymic architecture and T cell differentiation in SOD1-G93A (mSOD1) ALS mice at multiple disease stages. Thymocyte and thymic epithelial cells (TEC) subpopulations, as well as stages of Treg differentiation and suppressive capacity, were analyzed by flow cytometry, immunofluorescence, and functional assays. At late disease stage (120 days-old), mSOD1 mice displayed thymic atrophy, reduced thymocyte numbers, and decreased double-positive (DP), CD4 single-positive (SP), and Treg populations. Foxp3 expression per cell was preserved, but Treg progenitors and mature Treg numbers declined, paralleled by reduced suppressive function . TEC analysis revealed reduced total and mature medullary TEC (CD80MHCII), despite preserved Aire expression. Foxp3 cells were abnormally localized at cortical sites, away from mTEC, associated with migratory abnormalities and increased apoptosis. TREC evaluation revealed reduced intrathymic sjTREC, consistent with impaired proliferation and differentiation between DN and DP stages, although peripheral sj/βTREC ratios remained stable. Reduced Treg numbers were also observed in lymph nodes draining affected hindlimbs. Our findings identify the thymus as a target organ in ALS, where thymic involution, TEC loss, and Treg dysfunction may compromise immune tolerance. These alterations likely reinforce the role of the thymus in peripheral immune dysregulation and neuroinflammation observed in ALS. - Source: PubMed
Publication date: 2026/09/06
Lemos Julia PereiraStockholm DanielDinatale BrendaChaves Amanda SilvaPezet SoniaFrias Carvalho ViniciusPérez Ana RosaMendes-da-Cruz Daniella ArêasSavino WilsonSmeriglio Piera