CD86 Antibody
- Known as:
- CD86 Antibody
- Catalog number:
- 32223
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- CD86 Antibody
Related 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
- Atherosclerosis is a chronic inflammatory vascular disease. Circular RNAs (circRNAs) have emerged as important regulators of inflammatory processes, but their roles and regulatory mechanisms in atherosclerosis remain incompletely understood. This study aimed to investigate the role of circBRWD1 in atherosclerosis and its involvement in macrophage inflammatory responses. The expression and cellular localization of circBRWD1 were examined in high fat diet (HFD)-fed Apolipoprotein E knockout (ApoE) mice using qRT-PCR, fluorescence in situ hybridization (FISH) and immunofluorescence. The effects of AAV-mediated circBRWD1 knockdown on atherosclerotic lesions and plaque-associated inflammatory responses were evaluated in ApoE mice. The regulatory effects of circBRWD1 on macrophage inflammatory responses were further investigated in RAW264.7 macrophages using qRT-PCR, western blotting, ELISA and flow cytometry. The interaction between circBRWD1 and miR-141-5p and the regulation of HMGB1 by miR-141-5p were investigated using bioinformatic prediction, RNA pull-down, RNA immunoprecipitation, FISH, dual-luciferase reporter assays and functional rescue experiments. CircBRWD1 expression increased during atherosclerotic plaque development and was predominantly detected in macrophage-rich regions of advanced lesions. AAV-mediated circBRWD1 knockdown reduced aortic lesion size, plaque lipid accumulation, necrotic core area, TUNEL-positive signals and plaque-associated inflammatory markers in ApoE mice. In RAW264.7 macrophages, circBRWD1 preferentially modulated pro-inflammatory responses, including iNOS, CD86, and pro-inflammatory cytokine expression. Mechanistically, circBRWD1 interacted with miR-141-5p and modulated miR-141-5p-mediated regulation of HMGB1 and downstream NF-κB-associated inflammatory signaling. These findings identify circBRWD1 as a potential regulator of atherosclerotic plaque progression and macrophage inflammatory responses, and support the involvement of the miR-141-5p/HMGB1/NF-κB regulatory relationship in these effects. circBRWD1 may therefore represent a potential target for modulating plaque-associated inflammation in atherosclerosis. - Source: PubMed
Publication date: 2026/09/23
Wen ChengFang ZhiRuan YushuangMu HouyingDong ZikangTao EnxiangXia Yuanpeng - Non‑alcoholic steatohepatitis (NASH) is characterized by hepatic steatosis, inflammation, and fibrosis, yet therapeutic options remain limited. Aberrant activation of stimulator of interferon genes (STING) signaling in macrophages drives hepatic inflammation. Saikosaponin D (SSd), a bioactive triterpenoid saponin from Bupleurum falcatum, exhibits hepatoprotective properties, but its role in modulating STING-mediated macrophage polarization in NASH remains unknown. A NASH mouse model was established in C57BL/6J mice by feeding a methionine-choline-deficient (MCD) diet for 4 weeks, followed by 8 weeks of the MCD diet combined with SSd (10 mg/kg, oral gavage), polyene phosphatidylcholine (177.8 mg/kg, oral gavage), or the STING inhibitor C-176 (15 mg/kg, intraperitoneally). Hepatic injury, inflammation, and fibrosis were assessed by serum biochemistry, enzyme-linked immunosorbent assay, hematoxylin-eosin and Masson staining. Macrophage polarization status was analyzed by flow cytometry, qRT-PCR, and immunofluorescence, while STING pathway activation was quantified by qRT-PCR and Western blot. Molecular docking was performed using AutoDock Vina. SSd significantly attenuated MCD-induced hepatic steatosis, inflammation (reduced tumor necrosis factor-α and interleukin-6), and fibrosis. SSd decreased the proportion of hepatic M1 macrophages (F4/80CD86) while increasing M2 macrophages (F4/80CD206), alongside diminished colocalization between STING and F4/80. SSd markedly suppressed the expression and phosphorylation of STING, TBK1, IRF3, and nuclear factor-κB (NF-κB) at both the mRNA and protein levels, with efficacy comparable to that of C-176. Molecular docking revealed a strong binding affinity between SSd and STING (-9.9 kcal/mol). Collectively, SSd ameliorates NASH by inhibiting the STING-TBK1-IRF3/NF-κB axis in macrophages and promoting M1-to-M2 polarization, identifying SSd as a promising immunomodulatory therapy for NASH. - Source: PubMed
Zhang WenjieYin YaoCheng SiqiLi CaixiaCui LihuaChen Ming - Immune checkpoints (ICPs) are essential regulators of immune homeostasis, maintaining the balance between effective immune responses and tolerance to self-antigens. Dysregulation of ICP signaling may contribute to impaired immune surveillance, immune evasion, chronic inflammation, autoimmunity, persistent infections, and tumor progression. Consequently, ICP molecules are increasingly recognized not only as therapeutic targets but also as potential diagnostic, prognostic, predictive, and treatment-monitoring biomarkers. This review provides a comprehensive overview of the biological functions, signaling mechanisms, and clinical significance of major co-inhibitory and co-stimulatory ICP pathways, including PD-1/PD-L1/PD-L2, CTLA-4/CD28/CD80/CD86, LAG-3, TIM-3, TIGIT, BTLA, VISTA, ICOS, OX40, 4-1BB, GITR, CD27, CD40, and CD2, together with their corresponding ligands. Particular emphasis is placed on their biomarker potential in cancer and immune-mediated diseases. In addition, the review presents a bioinformatic characterization of ICP receptors and ligands based primarily on data available in UniProtKB and complementary bioinformatic resources. The analysis includes protein sequence length, molecular weight, theoretical isoelectric point, amino acid composition, subcellular localization, conserved and functional domains, protein family classification, post-translational modifications, isoforms, and selected structural features. Collectively, the available evidence indicates that ICPs constitute a structurally and functionally diverse group of immunoregulatory molecules with substantial biomarker potential. Integrating their molecular, structural, functional, and bioinformatic characteristics may improve disease classification, prognosis, patient stratification, treatment selection, and therapeutic monitoring. Such an integrated approach may also support the identification of novel biomarkers and therapeutic targets and contribute to the further development of precision and personalized medicine. - Source: PubMed
Publication date: 2026/09/09
Czosnek MilenaSowa AgataRolek ŁucjaGrywalska EwelinaMertowski SebastianMertowska Paulina - Blastocyst implantation is associated with quasi-inflammatory reactions in the endometrium, which are resolved during the establishment of the definitive placenta. Quasi-inflammatory processes have also been documented in pregnant pigs, even though the blastocyst only attaches to, rather than implants into the endometrium. We asked what processes lead to the resolution of attachment-associated inflammation. In wound healing the transition towards an anti-inflammatory state includes the transition from M1 to M2 polarized macrophages. In order to determine whether this scenario applies also to the peri-attachment porcine uterus, we produced a series of bulk transcriptomes spanning days 13 to 25 of gestation. We found slower changes in the transcriptome between D20 and D25 than prior to D20, suggesting a turning point in pregnancy-related endometrial reprogramming. This period corresponds to the firm attachment of trophectoderm to the uterine epithelium and the cessation of IFNG signaling from the blastocyst. We found increased expression of genes implicated in resolution of inflammation and M2 polarization such as ARG1, MRC1, CD86, TGFb1 and IL10, and an increase in expression of HGPD, the enzyme metabolizing prostaglandins. While immunoreactivity for ARG1 was found in putative macrophages, other M2 markers were localized to non-immune cells: MRC1 in fibroblast-like stromal cells, CD86 on trophoblast cells, and IL10 in endometrial epithelia. CD86 undergoes trogocytosis into the luminal epithelium by D25. These results suggest that intrauterine immune regulation is decoupled from that of the rest of the body by engaging non-immune cells as anti-inflammatory mediators during the peri-attachment period of porcine pregnancy. - Source: PubMed
Publication date: 2026/09/23
Wagner Günter PMinela ThaináRoss AlexandriaEngelhardt JanBazer Fuller WJohnson Gregory A - Loquat leaves (PPY) have long been used in traditional medicine for cough, phlegm, and wheezing-related respiratory disorders. However, the anti-asthmatic mechanisms of PPY, particularly those associated with airway inflammation and macrophage-derived inflammatory injury, remain incompletely understood. - Source: PubMed
Publication date: 2026/09/22
Zhang BeibeiZhao XinGuo YizhongZeng MengnanTie QimeiZheng XiaokeFeng Weisheng