CD86 Biotin
- Known as:
- CD86 Biotin
- Catalog number:
- ANT-284
- Product Quantity:
- 500µg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- CD86 Biotin
Related genes to: CD86 Biotin
- 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 Biotin
Related articles to: CD86 Biotin
- The long-term outcome of lung transplantation remains inferior to that of other solid organ transplants, primarily due to rejection/infection. This pilot study investigates longitudinal changes in the bronchoalveolar lavage (BAL) leukocyte transcriptomes and phenotypes, and their impact on clinical outcomes. - Source: PubMed
Publication date: 2026/05/18
Barbosa Vera MHu GuanganVaidyanathan ShrutiAkbariromani HaniehJustice SamuelMadsen JensSheikh AdilEl-Chemaly Souheil YSholl Lynette MarieCoppolino AnthonyMallidi Hari RElias Kevin MRoghanian AliChen JianzhuFrendl Gyorgy - As a leading cause of severe pulmonary infections, such as hospital-acquired pneumonia, (PA) poses a significant threat to public health. Macrophage polarization plays a central role in the control of PA infection; however, its precise regulatory mechanisms remain to be fully elucidated. It remains unclear whether MERTK participates in the regulation of macrophage polarization induced by PA infection, as well as its potential downstream molecular mechanisms, especially the association with the NLRC4 inflammasome. This study was designed to investigate the specific role and underlying molecular mechanisms of MERTK-mediated macrophage phenotypic switching during PA infection, with the goal of defining the MERTK-NLRC4 macrophage polarization regulatory axis. The expression dynamics of MERTK in alveolar macrophages from PA-infected mice were detected via Reverse transcription quantitative real-time PCR (RT‑qPCR) and Western blotting (WB). Flow cytometry was employed to determine the proportions of M1 (CD86+F4/80+) and M2 (CD206+F4/80+) macrophages. ELISA was utilized to quantify the levels of M1-associated (TNF-, IL-6) and M2-associated [IL-10, transforming growth factor (TGF)-] inflammatory cytokines, while the phagocytic activity of macrophages against PA was detected. WB was further applied to detect the expression of cleaved caspase-1 and N-GSDMD in the NLRC4 inflammasome pathway. The secretion of IL-1 and IL-18 and the release of lactate dehydrogenase were assessed. PA infection induced the upregulation of MERTK in alveolar macrophages. MERTK knockdown facilitated macrophage polarization toward the M1 phenotype while suppressing M2 polarization. Mechanistically, MERTK knockdown impaired NLRC4 inflammasome activation. Functional rescue experiments validated that MERTK overexpression activated M2 polarization by activating NLRC4 inflammasomes, which was reversed by NLRC4 knockdown. By upregulating MERTK to activate NLRC4 inflammasomes, PA facilitated M2 polarization of alveolar macrophages. This discovery furnished a critical theoretical foundation for the development of novel therapeutic strategies for PA infection targeting the MERTK-NLRC4 inflammasome-macrophage polarization axis. - Source: PubMed
Chen RongXu Yuanyuan - Mesenchymal stromal cells (MSCs) have shown enhanced therapeutic efficacy by cytokine pre-activation or licensing. Previous research has shown subconjunctival administration of low-dose allogeneic MSCs can significantly promote an anti-inflammatory phenotype. We report the effects of pro-inflammatory TNF-α/IL-1β MSC licensing, evaluating therapeutic potency in vitro and in a preclinical model of corneal alkali chemical burn. - Source: PubMed
Publication date: 2026/05/16
Canning AoifeDonohoe EllenJohnston ÉannaLynch KevinMoosavizadeh SeyedmohammadWang JieminLeahy MartinTreacy OliverRyan Aideen ERitter Thomas - Trillium tschonoskii Maxim. (TTM) is a traditional Chinese medicinal herb historically employed to enhance functional recovery in patients with cerebrovascular disorders, particularly during post-stroke rehabilitation. - Source: PubMed
Publication date: 2026/05/15
Wang HanyuXiao ZhongxinWang TingJia JingtingLei JianfengZhuang YumingZhao HuiYang Le - 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