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
- Microglia-mediated inflammation plays a critical role in secondary brain injury following ischemic stroke. Glycogen synthase kinase-3β (GSK-3β) and hexokinase 2 (HK2) are involved in regulating microglial inflammatory responses and can promote the release of pro-inflammatory factors under ischemic and hypoxic conditions, thereby exacerbating brain damage. Early exercise intervention has been shown to improve post-stroke neuroinflammation, but whether it exerts this effect by modulating GSK-3β/HK2-associated inflammatory signaling in microglia remains unclear. This study aimed to investigate the effects of early exercise on microglial inflammation and the potential involvement of GSK-3β/HK2 signaling. A twenty-eight-day early exercise regimen was applied in a rat model of middle cerebral artery occlusion (MCAO), and complementary in vitro experiments were conducted using BV2 microglial cells under oxygen-glucose deprivation. Results demonstrated that early exercise significantly improved neurological outcomes and reduced brain tissue damage, accompanied by decreased expression of microglial pro-inflammatory factors (IL-6, TNF-α, CD86, and iNOS) and increased levels of anti-inflammatory factors (IL-10 and Arg1). In vitro, inhibition of GSK-3β in BV2 cells markedly alleviated inflammatory responses under hypoxic conditions. In conclusion, early exercise intervention can attenuate post-stroke neuroinflammation, potentially by modulating GSK-3β/HK2 signaling in microglia to regulate. - Source: PubMed
Publication date: 2026/08/02
Li NaiWei YaWu HongyiYuan KeLi ChenHu JiayiWu XinyueZhang HaoboChen XinWan Chunxiao - Deficient IL10 signaling can contribute to macrophage activation syndrome. We hypothesized that in TLR-9-mediated inflammation, blocking IL10 would increase T cell activation and worsen organ dysfunction. - Source: PubMed
Publication date: 2026/08/05
Fisler GraceEremita MatthewChhabra ShivaniBrewer Mariana RQi MeiYuen Joyce HuiDeutschman Clifford STaylor Matthew D - Primary resistance to programmed cell death protein 1 (PD1) blockade is sustained by defective antigen presentation, immunosuppressive myeloid programs, regulatory T-cell (Treg) dominance, and dysfunctional lymphocyte states. Tumor Treating Fields (TTFields) are non-ionizing alternating electric fields with established antiproliferative activity; however, whether they can overcome resistance to immune checkpoint blockade remains unclear. - Source: PubMed
Publication date: 2026/08/06
Hu YunMaspourour FatemehWang QiHuang AilingBarsoumian HampartsoumRafiq ZahidHoffman AshleyRobinson DentonWang JingWelsh James W - Neuroinflammation is recognized as a contributing factor to cognitive disorders. Previous studies have demonstrated PHD3 drives microglia-mediated neuroinflammation. Present study aims to further clarify the role of PHD3 in both lipopolysaccharide (LPS)- and anesthesia/surgery (AS)-induced neuroinflammation and cognitive impairments. - Source: PubMed
Publication date: 2026/08/19
Che JiDeng YixuZhang XiangShi ChangshengHe ZhiyongDong JingZhang Jun - Diabetic foot ulcers (DFUs) arise within a dysregulated wound microenvironment in which sustained inflammation, bacterial susceptibility, and excessive oxidative stress collectively impede tissue repair. To address these interrelated barriers, we developed an asiaticoside-loaded silk fibroin/hyaluronic acid composite hydrogel (ASHF) as a bioactive dressing that couples structural support with localized drug delivery. By optimizing the mass ratio of its components, the resulting hydrogel achieved an excellent balance among mechanical compliance, swelling capacity, tissue adhesion, water vapor transmission rate, and enzymatic degradation. In vitro experiments demonstrated that ASHF released asiaticoside in a two-stage manner, was well tolerated by fibroblasts, promoted cell migration, and inhibited Escherichia coli and Staphylococcus aureus. In vivo evaluation in a diabetic mouse model revealed that ASHF-treated wounds closed more rapidly and showed stronger collagen deposition, CD31-positive neovascularization, and re-epithelialization. Dual immunofluorescence staining demonstrated a significant reduction in M1 macrophages (CD68/CD86) and a concurrent increase in M2 macrophages (CD68/CD206), alongside favorable shifts in local cytokines (decreased IL-6 and increased IL-10). These findings indicate an effective transition of the local immune microenvironment from persistent inflammation toward a pro-reparative state. Transcriptomic analysis of wound tissues further indicated that ASHF intervention was associated with enrichment of glutathione-related metabolic programs and epidermal differentiation signatures, together with upregulation of key genes including Gstm3, Aox4, Hal, and Krt1. These results suggest that ASHF supports diabetic wound repair through coordinated regulation of redox balance, macrophage polarization, and tissue reconstruction, highlighting its potential as a multifunctional dressing for chronic diabetic wounds. - Source: PubMed
Publication date: 2026/08/19
Liu XinyuLuo SiyiZhang HaiyangXiong XingliangSu AihuaLiang BoJiang Qifeng