Rat Anti-Mouse CD86, Biotinylated
- Known as:
- Rat Antibody toMouse CD86, Biotinylated
- Catalog number:
- 128-10055-2
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rat Anti-Mouse CD86 Biotinylated
Related genes to: Rat Anti-Mouse CD86, Biotinylated
- 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: Rat Anti-Mouse CD86, Biotinylated
Related articles to: Rat Anti-Mouse CD86, Biotinylated
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Eteghadi AtefehTaghipour NiloofarHosseinzadeh SimzarHashemi Seyed MahmoudGhasemi Fatemeh SadatSoleimani Masoud - Pectic polysaccharides from medicinal plants are promising natural immunomodulators, but their structural heterogeneity has hindered the identification of bioactive domains and limited their further development. The structural basis underlying their regulation of dendritic cell-mediated immune responses remains poorly understood. - Source: PubMed
Publication date: 2026/09/28
Xu YongbinGuo MengyaLiu YupengChen JieShi SongshanShi ChenchenWang ShunchunWang Huijun - 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
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