Ask about this productRelated genes to: CD86 antibody
- Gene:
- CD86 NIH gene
- Name:
- CD86 molecule
- Previous symbol:
- CD28LG2
- Synonyms:
- B7.2, B7-2
- Chromosome:
- 3q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-07
- Date modifiied:
- 2016-10-05
Related products to: CD86 antibody
Related articles to: CD86 antibody
- Hypervirulent (hvKP) causes invasive infections, including bloodstream infections and liver abscesses, and dysregulated host inflammation may exacerbate liver injury. We investigated whether pretreatment with Humanin, a mitochondria-derived anti-inflammatory peptide, could attenuate hvKP-associated liver injury. We measured serum Humanin in 20 patients with hvKP-associated bloodstream infection and liver abscess and 20 matched healthy controls. C57BL/6 mice received intraperitoneal Humanin (2.5 or 5 mg/kg/day) for five days before intravenous hvKP challenge. We assessed liver injury, inflammatory responses, hepatic transcriptomes, NF-κB activation, and survival. Serum Humanin was higher in patients than in the controls ( < 0.001). In infected mice, Humanin pretreatment was associated with less prominent histopathological liver injury and lower serum ALT, AST, and PCT, hepatic myeloperoxidase activity, F4/80 immunoreactivity, CD86 fluorescence, and pro-inflammatory gene expression. The effects were generally greater at 5 mg/kg than at 2.5 mg/kg. Transcriptomic analysis showed attenuation of inflammatory pathways, including NF-κB signaling (NES = -1.86, = 0.002, FDR = 0.012). Humanin also reduced p-p65/p65 and p-IκBα/IκBα ratios in liver tissue and hvKP-stimulated bone-marrow-derived macrophages; 5 mg/kg prolonged survival ( < 0.05). Humanin pretreatment may therefore limit inflammatory liver injury during systemic hvKP infection. This effect was associated with reduced macrophage-associated inflammation and NF-κB activation, although its molecular targets remain unknown. - Source: PubMed
Publication date: 2026/09/10
Zhong YimingHaishaer DinaCai WeidongLin LinGuo ZhaopeiPan YanTang XiangjunYou WeiquanFu YaOu Qishui - A water-soluble, low-molecular-weight polysaccharide fraction, designated OJP-2, was extracted from the roots of ; its structural characteristics and immunomodulatory activity in macrophages were subsequently investigated. OJP-2 exhibited a narrow apparent molecular weight distribution with an average molecular weight (Mw) of 3568 Da and was primarily composed of fructose (0.784) and glucose (0.208). Structural analysis-integrating UV spectroscopy, Fourier-transform infrared (FT-IR) spectroscopy, and 1D/2D nuclear magnetic resonance (NMR) spectroscopy-revealed that OJP-2 is an inulin-type fructan. Its structure is characterized predominantly by β-(2→1)-linked Fruf chains and terminal α-D-Glcp residues, with potential signals indicating C-6-substituted Fruf units. In vitro immunological studies demonstrated that OJP-2 promoted nitric oxide (NO) production and enhanced the secretion of IL-6, IL-1β, and TNF-α in RAW264.7 macrophages. Under LPS/IFN-γ stimulation, OJP-2 induced non-monotonic changes in the CD86/CD206 macrophage phenotype, with the most pronounced effects observed at a concentration of 50 μg/mL. Furthermore, Western blot analysis showed that, compared to the Model group, treatment with OJP-2 resulted in a downward trend in the relative levels of p-p65/p65 and p-IκBα/IκBα across the tested concentration range. Collectively, these findings indicate that OJP-2 modulates macrophage activation phenotypes and influences NF-κB-related signaling pathways. Thus, OJP-2 is a candidate fructan for further investigation of immunomodulatory activity. - Source: PubMed
Publication date: 2026/09/10
Sun HenanYu HaoYu HuiqiangSaren GaowaFeng KeHu Wenzhong - subsp. (SEZ) causes severe infections, but the role of the negative regulator interleukin-1 receptor-associated kinase M (IRAK-M) in SEZ-induced inflammation is unclear. In this study, male C57BL/6 mice received a single intraperitoneal injection of SEZ at 2 × 10 CFU and were examined 24 h post-injection. SEZ infection triggered overt jejunal hemorrhage and upregulation of IL-1β, IL-6, and TNF-α mRNA, confirming local inflammation, with a concurrent marked reduction in both mRNA and protein levels of IRAK M in the jejunum, hinting at its possible role. We next used IRAK-M knockout (IRAK-M) mice and found that, compared with the WT+SEZ group, the knockout group displayed more severe jejunal hemorrhage, histopathological scores, and neutrophil infiltration, along with a higher bacterial burden and further elevated pro-inflammatory cytokines and reduced anti-inflammatory cytokine expression. Mechanistically, IRAK-M deficiency in the jejunum further increased the mRNA expression of MyD88, TRIF, TRAF6, IKKα+β, NF-κBp50, and NF-κBp65 and decreased IκBα mRNA compared with the WT+SEZ group. These findings were paralleled at the protein level, as demonstrated by Western blotting for MyD88, TRAF6, and IKKα+β, and by immunofluorescence in peritoneal macrophages. Importantly, IRAK-M deficiency drove a shift toward the M1 macrophage phenotype in both jejunal tissues and peritoneal macrophages, characterized by upregulation of CD16, CD32, CD80, CD86, iNOS, and MHC II, and downregulation of the M2-associated markers Arg1 and CD206. These findings reveal that SEZ infection causes jejunal inflammation and that IRAK-M knockout worsens this condition, pointing to a role for IRAK-M in regulating inflammatory readouts in this model. - Source: PubMed
Publication date: 2026/09/16
Che YuxinXie YiQiu XinyiLin JunxiXiu YixinYu TaoyuZhan XiaoshuLiao JiedanHuang YunfeiYe YaqiongDeng Ziteng - Cancer immunotherapy faces significant challenges in treating "cold" tumors, which respond poorly to current strategies. Breast cancer is a major cause of cancer-related mortality in women and is a representative immunosuppressive cold tumor. The luminal A subtype of breast cancer exhibits an immune-cold phenotype, with MCF-7 cells used as a representative cell model. Here, we identified (3β,5α,8α)-5,8-epidioxyergost-6-en-3β-ol (EEO), isolated from , as an inducer of immunogenic cell death (ICD) hallmarks in MCF-7 cells, including cell surface exposure of calreticulin (CRT) and the extracellular release of damage-associated molecular patterns (DAMPs), such as ATP and High Mobility Group Box 1 (HMGB1). These ICD-associated events subsequently promoted CRT-dependent dendritic cell (DC) activation in a co-culture system with bone marrow-derived DCs and MCF-7 cells. Furthermore, surface-exposed CRT enhanced the phagocytosis of EEO-treated MCF-7 cells by DCs, and this phagocytic activity promoted DC maturation, as indicated by increased cell surface levels of the maturation markers major histocompatibility complex class II (MHC II) and cluster of differentiation 86 (CD86). Moreover, CRT knockdown in MCF-7 cells reduced surface CRT exposure following EEO treatment, thereby suppressing DC-mediated phagocytosis and subsequent DC maturation. Taken together, these findings suggest that EEO is a promising candidate for enhancing the antitumor efficacy of existing breast cancer immunotherapies through ICD-mediated DC maturation and converting immunologically cold tumors into hot tumors. - Source: PubMed
Publication date: 2026/09/02
Shin Seong-AhMoon Sun YoungChoi SeyeonKim MinjiKim MoonsuLee Jun HyuckLee SeulahKim Ki HyunPark Hyun HoYoun Ui JoungLee Chang Sup - Atherosclerosis is a chronic immune-inflammatory disease of the arterial wall in which antigen-presenting cells (dendritic cells, macrophages and B cells) present locally generated antigens, such as oxidized low-density lipoprotein, to plaque-infiltrating T cells. Full T-cell activation requires costimulation through the B7 family ligands CD80 (B7-1) and CD86 (B7-2), which engage CD28 to activate T cells and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) to restrain them. Although long considered functionally redundant, CD80 and CD86 are now known to be structurally and mechanistically distinct, differing in receptor affinity, susceptibility to CTLA-4-mediated trans-endocytosis, capacity to cis-heterodimerize with programmed death-ligand 1, and dependence relationships with regulatory versus effector T cells. In atherosclerosis, CD80 is expressed by lesional dendritic cells, macrophages, foam cells, B cells and, under inflammatory conditions, vascular endothelial and smooth muscle cells, with expression levels correlating with plaque vulnerability in humans. Genetic deletion, CTLA-4-Ig-based pharmacological blockade and selective small-molecule antagonism in preclinical models generally converge on a proatherogenic role for CD80/CD86-dependent costimulation, although combined genetic deletion of CD80 and CD86 has also been reported to paradoxically enhance early lesion formation in some contexts, while augmented CTLA-4-mediated coinhibition is atheroprotective-a balance corroborated by the accelerated atherosclerosis and cardiovascular toxicity observed with checkpoint-inhibitor cancer immunotherapy. Molecular imaging agents targeting CD80/CD86, repurposed CTLA-4-Ig biologics such as abatacept, and antigen-specific tolerogenic dendritic cell strategies together constitute an emerging translational pipeline. To our knowledge, this is the first review to integrate CD80's structural and receptor pharmacology with its cellular sources in the plaque, preclinical genetic and pharmacological evidence, human plaque and biomarker data, molecular imaging approaches, and checkpoint inhibitor-associated cardiovascular toxicity within a single translational framework. This review synthesizes the structural biology, cellular sources, preclinical genetics, human plaque and biomarker data, and therapeutic and diagnostic implications of CD80 as an immune mediator and candidate therapeutic target in atherosclerosis. - Source: PubMed
Publication date: 2026/09/15
Blagov AlexanderVatlin AlekseyBorodko DariaMaksaeva Anastasia