Rat Anti-Mouse CD86
- Known as:
- Rat Antibody toMouse CD86
- Catalog number:
- 128-10054-1
- Product Quantity:
- 500
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rat Anti-Mouse CD86
Related genes to: Rat Anti-Mouse 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: Rat Anti-Mouse CD86
Related articles to: Rat Anti-Mouse CD86
- The immunosuppressive bone marrow microenvironment (BMM) and cytokine dysregulation remain major barriers to curing multiple myeloma (MM). Despite the promise of B-cell maturation antigen (BCMA)-targeted therapies, their clinical utility is often limited by antigen escape and insufficient immune activation. Here, we developed DB Exo, a cell-free therapeutic platform utilizing allogeneic dendritic cell-derived exosomes engineered to surface display BCMA. Mechanistically, DB Exo act as molecular decoys that predominantly sequester soluble APRIL with partial BAFF attenuation, thereby effectively disrupting NF-κB pro-survival signaling in MM cells. Concurrently, DB Exo retain inherited costimulatory molecules (CD80, CD86, and MHC-II) to trigger strong host immune activation, expanding CD8 T cells and enhancing the secretion of cytotoxic effector molecules. In an orthotopic murine model, DB Exo suppress tumor burden by ∼72% and remodel the BMM by increasing cytotoxic T-lymphocyte infiltration and elevating serum IFN-γ and Granzyme B levels. The robust antitumor efficacy was further validated in a subcutaneous model, with DB Exo achieving a ∼75% reduction in tumor weight. Our findings establish DB Exo as a potent bi-functional exosome platform that integrates targeted cytokine blockade with in situ immune activation, offering a promising cell-free strategy for MM treatment. - Source: PubMed
Publication date: 2026/05/15
Zeng YuqingHe ChaoHe ZhibinChen HongboCheng FangZheng Yongjiang - Hypersensitivity pneumonitis (HP) is characterized by bronchiolocentric inflammation and fibrosis. The characteristic pathological features include bronchiolocentric inflammation, peribronchiolar fibrosis, and the presence of poorly formed granulomas. Nerandomilast is a novel oral phosphodiesterase 4 (PDE4) inhibitor with good selectivity for PDE4B. PDE4 inhibitors (PDE4i) exhibit anti-inflammatory/antifibrotic properties, the efficacy of nerandomilast remains unexplored in HP. - Source: PubMed
Publication date: 2026/05/14
Shi YujieLiu YumingLiu ZhigangChen RuxuanWang MengqiLi ZhiyiChen QiShao ChiLi XiaoheZhou HonggangHuang Hui - Obesity-associated metabolic inflammation is characterized by the infiltration and pro-inflammatory polarization of adipose tissue macrophages (ATMs). Mitochondrial dysfunction represents a central pathogenic mechanism; however, the upstream molecular mechanisms that link metabolic stress to impaired mitochondrial quality control in macrophages remain inadequately defined. Regulator of G protein signaling 1 (RGS1) is significantly upregulated in ATMs under obese conditions; nevertheless, its functional role and mechanistic relevance have not been fully elucidated. - Source: PubMed
Publication date: 2026/05/13
Li YunmengFu XuanYin BaolongNasrin MahbubaHuo Rui - Melanoma is a highly aggressive malignancy characterized by limited immunogenicity and pronounced immune evasion, which represent significant obstacles to effective therapeutic intervention. Building on our previously developed multifunctional PDA-Ce6-R837 nanoparticles (NPs), which have demonstrated favorable antitumor efficacy in squamous cell carcinoma (SCC) models, the present study shifts focus toward elucidating their underlying photo-immunological mechanisms in melanoma cells. Here, we investigate their antitumor and immunoregulatory effects in melanoma cell models. studies demonstrated the efficient internalization of PDA-Ce6-R837 NPs by SK-Mel-28 and A375 cells, which was accompanied by pronounced photothermal and photodynamic responses. Functional assays revealed that this treatment markedly suppressed cell migration and invasion and, under dual-wavelength laser irradiation, significantly induced apoptosis while promoting key hallmarks of immunogenic cell death (ICD), including the translocation of calreticulin (CRT) and the extracellular release of adenosine triphosphate (ATP) and high-mobility group box 1 (HMGB1). In coculture systems, treatment with R837 alone promoted the maturation of bone marrow-derived dendritic cells (BMDCs), whereas laser activation of PDA-Ce6-R837 NPs enhanced BMDC maturation, as evidenced by further upregulation of CD80/CD86 expression and increased IL-12p70 production. Collectively, these findings demonstrate that PDA-Ce6-R837 NPs combine direct cytotoxic effects with immune stimulation in melanoma phototherapy, offering experimental evidence to support the development of phototherapy-based immunotherapeutic strategies for melanoma. - Source: PubMed
Publication date: 2026/05/12
Wang JianvLiu ChenxiZhang XiaoyanXie YaoZhang XueyuWang TingtingWang Lin - The underlying proinflammatory mechanism of coagulation factor VⅡ in coronary artery disease (CAD) remains unclear. According to the inclusion criteria, 24 non-CAD subjects and 24 patients with CAD were enrolled. The expression levels of pro-inflammatory (CD14CD86, CD14CD163), anti-inflammatory monocytes (CD14CD163), CD14CD142 and CD14PAR2 monocytes in peripheral blood were detected by flow cytometry. The levels of TNF-α, IL-1β, IL-6, IL-10, and FVⅡ in plasma were determined by ELISA. In vitro experiments were conducted to induce inflammatory THP-1 by FVⅡa. The FVⅡa/TF complex inhibitor PCI-27,483 and PAR2 antagonist AZ3451 were used to clarify the mechanisms. Compared with the control group, the percentage of CD14CD86 pro-inflammatory monocytes were significantly increased in the CAD group, and further elevated after PCI. The results of the levels of CD14CD142 and CD14PAR2 monocytes showed the same trends with CD14CD86 pro-inflammatory monocytes. The levels of CD14CD163 anti-inflammatory monocytes and IL-10 were decreased in CAD patients, but increased after PCI. The pro-inflammatory factors and FVⅡ were significantly elevated in the CAD group and significantly decreased after PCI. Correlation analysis revealed that FVⅡ, TF, and PAR2 were significantly associated with CD14CD86 pro-inflammatory monocytes, and inflammatory factors. In vitro studies further confirmed that the FVⅡa/TF coagulation complex and PAR2 could activate NF-κB in monocytes and aggravate inflammation. Our findings suggest that crosstalk between monocytes and the coagulation complex might contribute to residual inflammation in CAD, potentially involving the FVIIa/TF/PAR2-NF-κB signaling pathway. Based on these observations, we hypothesize that blocking the interaction between clotting factors and monocytes could represent a promising therapeutic strategy to mitigate residual inflammation, but further rigorous experiments are needed for verification. - Source: PubMed
Publication date: 2026/05/14
Wang BaofuHan WenboXiu ShengyaoLi YangHan XiaowanZhao MingjingWang Xian