CD86
- Known as:
- CD86
- Catalog number:
- 1P-531-T025
- Product Quantity:
- 25 tests
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD86
Related genes to: CD86
- 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
Related articles to: CD86
- Vascular regenerative cell exhaustion (VRCE), a shift in the circulating progenitor cell profile, has been linked with adverse cardiometabolic outcomes. Whether VRCE is also involved in the pathogenesis and vascular repair mechanisms of peripheral artery disease (PAD) is unknown. In this study, we sought to compare the circulating vascular regenerative cell content of adults living with PAD with those without PAD. - Source: PubMed
Publication date: 2026/08/17
Casey Jack HMoroney MichaelTeoh HweeKrishnaraj AishwaryaQuan AdrianPan YiDennis FallonHe Arianna ZPark BradyVerma RajMisner ElizabethAli Hassan Syed MDennis Cole JMeglis GusMazer C Davidde Mestral CharlesHussain Mohamad ARoche-Nagle GrahamCurley Gerard FHess David AVerma Subodh - Bacillus Calmette-Guérin (BCG) remains the only licensed vaccine for tuberculosis (TB), yet its efficacy wanes over time due to insufficient durability of vaccine-induced immunity. However, mechanisms constraining BCG vaccine-induced dendritic cell (DC)-mediated T cell priming are poorly understood. Cholesterol 25-hydroxylase (CH25H) converts cholesterol into 25-hydroxycholesterol (25-HC) that modulates antigen-presenting cell imprinting and innate immune responses. Here, we investigated whether CH25H regulates DC function and vaccine-induced protective immunity against (Mtb). We found that CH25H deficiency enhanced DC activation, characterized by increased expression of the costimulatory molecules CD80 and CD86, elevated interleukin (IL)-12p70 production, and reduced IL-10 secretion, resulting in augmented T cell proliferation and robust Th1 cytokine responses. Transcriptomic analyses of CH25H-deficient and 25-HC-treated DCs showed that an SREBP2-associated program may contribute to expression. BCG vaccination conferred enhanced protection in mice, including reduced Mtb burden and pulmonary inflammation. BCG-vaccinated mice developed more durable protective immunity and increased frequencies of CD103CD69 tissue-resident memory T cells, along with sustained IL-2-producing T cell responses. Collectively, these findings identify CH25H as a negative regulator of DC-mediated Th1 immunity and suggest that targeting CH25H represents a potential host-directed immunomodulatory strategy to enhance the long-term protective immunity of TB vaccination. - Source: PubMed
Publication date: 2026/09/30
Kim HagyuChoi EunsolKwon Kee WoongChoi Hong-HeeKim KyungminJung WeonSeokShin Sung Jae - The immunomodulatory activity of normothermic machine perfusion (NMP) on donor organs may be reflected by the release of immune-regulating factors into the perfusate. Dendritic cells (DCs) are potent antigen-presenting cells and are able to sense these factors. We hypothesized that activation of DCs could be used to monitor the release of these mediators into the perfusate. - Source: PubMed
Publication date: 2026/09/30
Knijff Laura W DArykbaeva Asel Svan der Kooij Sandra Wde Vries Dorottya Kvan Essen Mieke FAlwayn Ian P JLeuvenink Henri G DPloeg Rutger Jvan Kooten Cees - Ischemic stroke (IS) triggers neuroinflammation cascades where microglial polarization is a pathological determinant. Mailuoning oral liquid (MLN O) is clinically utilized to prevent thrombosis and treat convalescent IS, but its pharmacological targets in permanent IS remain unclear. - Source: PubMed
Publication date: 2026/09/30
Liu XiaoqiongLin YandanLi JianJiang HongSui YihangLi YueyuanFan LinglingChen HaiTan Ninghua - This study describes a protocol integrating network pharmacology and in vitro experiments to evaluate the protective effects of Huangqin Tang (HQT) and one of its bioactive constituents, paeoniflorin (PF), against oxidized low-density lipoprotein (ox-LDL)-induced macrophage dysfunction and to investigate AMP-activated protein kinase (AMPK)-related signaling. Network pharmacology identified HQT targets and pathways associated with atherosclerosis (AS). An ox-LDL-induced RAW264.7 macrophage model was used to assess lipid accumulation, cholesterol efflux, adenosine triphosphate (ATP) levels, inflammatory responses, mitochondrial function, oxidative stress, apoptosis, and macrophage phenotypic markers. HQT and PF were compared at non-cytotoxic concentrations. AMPK involvement was evaluated using a cell thermal shift assay (CETSA), pharmacological inhibition, and small interfering RNA (siRNA)-mediated knockdown. ATP-binding cassette transporter A1 (ABCA1), liver X receptor alpha (LXRα), nuclear factor kappa B (NF-κB)-related proteins, and apoptosis-associated proteins were examined by western blotting. Network pharmacology identified 12 overlapping targets, including TNF, PPARG, and NOS3, enriched in pathways related to lipid metabolism, inflammation, AS, and AMPK signaling. Both PF and HQT increased AMPK phosphorylation, reduced ox-LDL-induced lipid accumulation and inflammatory cytokine secretion, and improved cholesterol efflux. PF restored ATP levels and mitochondrial membrane potential, reduced reactive oxygen species production and apoptosis, and increased ABCA1 expression. CETSA demonstrated enhanced AMPK thermal stability following PF treatment. Pharmacological inhibition or siRNA-mediated knockdown of AMPK attenuated PF-associated changes in ABCA1 expression, cholesterol efflux, lipid accumulation, LXRα activation, and NF-κB inhibition. PF reduced CD86⁺ macrophages and increased CD206⁺ macrophages, whereas AMPK silencing partially reversed these changes. NF-κB inhibition produced similar effects on cholesterol homeostasis and macrophage phenotypic markers. This protocol enables evaluation of PF- and HQT-mediated effects on ox-LDL-induced macrophage dysfunction and AMPK-related signaling. Under the tested conditions, PF protected RAW264.7 cells against ox-LDL-induced lipid metabolic dysfunction, inflammation, oxidative stress, mitochondrial dysfunction, and apoptosis, and PF and HQT produced directionally similar changes in macrophage-related endpoints. - Source: PubMed
Publication date: 2026/09/29
Zeng YunjieWang HuayingLiu DongJiang YunluRen PengchengSong WenxinHuang GuopengHe Xiaojiao