Recombinant human CD86 /B7-2 Protein
- Known as:
- Recombinant H. sapiens CD86 /B7-2 Protein
- Catalog number:
- cd-737
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant human CD86 /B7-2 Protein
Related genes to: Recombinant human CD86 /B7-2 Protein
- 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
- Gene:
- GIPC3 NIH gene
- Name:
- GIPC PDZ domain containing family member 3
- Previous symbol:
- C19orf64, DFNB72, DFNB15
- Synonyms:
- DFNB95
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-06-28
- Date modifiied:
- 2015-11-18
- Gene:
- STOM NIH gene
- Name:
- stomatin
- Previous symbol:
- EPB7, EPB72
- Synonyms:
- BND7
- Chromosome:
- 9q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-14
- Date modifiied:
- 2016-10-05
Related products to: Recombinant human CD86 /B7-2 Protein
Related articles to: Recombinant human CD86 /B7-2 Protein
- Functional impairment of T and NK cells following irradiation (IR) undermine anti-tumor immune responses. This study aimed to investigate the characteristics of T-cell and NK-cell reconstitution in mice following low-dose radiation-induced injury and the restorative effects of Rehmanniae Radix Praeparata (RRP). At various time points post-IR, splenic/thymic indices, complete blood count and CD3+ T, CD4+ T, CD8+ T and NK cells, as well as CD80, CD86, MHC-I and MHC-II were assessed. Type 1 T helper (Th1), Type 1 cytotoxic (Tc1), Type 1 NK (NK1), regulatory T (Treg) and Th17 cells along with IL-12, IL-15, T-bet and foxP3 were also evaluated with or without RRP treatment. Additionally, a B16 melanoma lung metastasis model in irradiated mice was used to confirm the restorative effects of RRP. CD3+, CD4+, CD8+ T and NK cells decreased significantly on Days 4 to 6 and largely recovered by Days 9 to 11 post-IR. The expression of CD80, CD86 and MHC-II reduced on Day 6 and recovered by Day 11. However, interferon (IFN)-γ production by Th1, Tc1 and NK1 cells remained lower, whereas Tregs were elevated. RRP effectively enhanced IFN-γ production from Th1, Tc1 and NK1 cells and suppressed Tregs by increasing T-bet and decreasing foxP3 expression, thereby significantly reduced the tumor burden. These findings suggest that T-Cell and NK-Cell-mediated inefficient reconstitution following IR was characterized by an decrease of Th1, Tc1 and NK1 cells and an increase of Tregs, RRP effectively promoted the functional reconstitution of T-cell and NK-cell subsets, thereby enhancing anti-tumor immunity after IR. - Source: PubMed
Publication date: 2026/04/22
Zheng XiaodanLan HongyunHu YuhaiQiu TianyunHou HairuiTian Peifu - Bone graft rejection in oral surgery remains a significant challenge, potentially compromising the success of reconstructive procedures. Biomaterial-associated molecular patterns (BAMPs) play a pivotal role in bone graft integration and rejection by initiating and modulating immune responses during the foreign body reaction (FBR). This study evaluated BAMPs components, physicochemical properties, and adsorbed serum proteomic profiles in demineralized (DMB) and decellularized (DCC) bone grafts. The immunomodulatory effect of adsorbed serum proteins on DMB and DCC to modulate macrophage polarization was also investigated. Serum protein adsorption profiles were determined by incubating 0.5 g of DMB and DCC bone grafts in 10% FBS. Adsorbed serum proteins were buffer-desorbed, quantified, and subjected to proteomic analysis. The capacity of DMB and DCC adsorbed serum proteins to modulate functional and phenotypic profiles of macrophages was assessed using THP-1 cells. Macrophages were incubated for 72 hours with or without DMB- or DCC-adsorbed serum proteins, followed by expression analysis of CD14, CD16, CD86, CD206, HLA-DR, iNOS, Arg-1, IL-1β, TNF-α, IL-10, and TGF-β. Physicochemical analysis revealed that DCC bone grafts' surfaces were hydrophilic, anionic, and smooth, whereas DMB surfaces were hydrophobic, mildly anionic, and rough. The proteomic profiles of adsorbed serum proteins associated with DMB and DCC bone grafts showed significant variations. Macrophages exposed to DCC-adsorbed serum proteins exhibited an elongated cell morphology, increased expression of CD16 and CD206 (p < 0.0001), and higher Arg-1 expression. Conversely, the DMB group macrophages exhibited a rounded cell morphology, increased expression of CD86 and HLA-DR (p < 0.01), and higher iNOS expression. The DCC group showed higher mRNA levels of IL-10 and TGF-β (p < 0.0001). The physicochemical properties of bone grafts govern serum protein adsorption, which, in turn, directs macrophage polarization and graft acceptance. Understanding these interactions guides the design of immunomodulatory biomaterials to enhance graft integration. - Source: PubMed
Publication date: 2026/04/21
Brigi CarelHamad MawiehAli Abou Neel EnsanyaSelvakumar BalachandarRani K G AghilaAlKawas SausanAl Hroub Hamza MJemimah SherlynMajdalawieh Amin FMahasneh AmjadSamsudin A R - Delayed cerebral ischemia remains a major determinant of poor outcomes after aneurysmal subarachnoid hemorrhage (SAH), yet effective preventive strategies are limited. The gut-brain axis has emerged as an important modulator of post-SAH neuroinflammation and vascular dysfunction. We hypothesized that pre-existing gut microbiome dysbiosis (GMD) exacerbates neuroinflammation and vasospasm after SAH. - Source: PubMed
Publication date: 2026/04/21
Matsukawa HidetoshiFujita MitsuguKuramoto YojiKuwahara ShuntaroTsuji ShoichiroTakeda YukiSon AoiKato TamotsuShirakawa ManabuYoshimura Shinichi - Inflammation is associated with various cancers, including colorectal cancer. Momordin Ic (MIc) has anti-tumor and anti-inflammatory properties, but its effects on colitis-associated colorectal cancer (CAC) are not well understood. This study explores MIc's influence on macrophage mitochondrial dysfunction, macrophage polarization, and tumor development in CAC. Mouse colitis and CAC models were established to assess MIc's therapeutic potential. H&E staining and immunohistochemistry evaluated inflammation and mucosal damage in colonic tissues. Flow cytometry analyzed immune cell proportions, while Western blot analyzed inflammatory protein expression. In vitro studies with RAW264.7 and BMDMs explored MIc's effects on macrophage polarization and mitochondrial function. Flow cytometry assessed CD86+ macrophages, and qRT-PCR measured inflammatory cytokines. Mitochondrial function was assessed using Mito-tracker, JC-1, and DCFH-DA dyes. Proteomics and GO analysis identified downstream pathways. Flow cytometry and CCK-8 assessed colon cancer cell proliferation and apoptosis, confirmed in the CAC mouse model. MIc significantly reduced intestinal inflammation and mucosal damage by decreasing macrophage infiltration and pro-inflammatory polarization. Proteomics revealed that MIc affected proteins related to mitochondrial function. MIc restored mitochondrial function impaired by M1 polarization through upregulation of MTCH2. Co-IP analysis showed a direct interaction between Sentrin-specific protease 1 (SENP1) and MTCH2. SENP1 levels increased in M1 macrophages but decreased with MIc, an effect blocked by NFκB inhibitors. MIc promoted apoptosis in CT26 and HCT116 cells and inhibited CAC progression. MIc effectively suppresses CAC development by regulating macrophage mitochondrial function via the SENP1/MTCH2 pathway, reducing M1 polarization and promoting apoptosis in colorectal cancer cells. - Source: PubMed
Publication date: 2026/04/20
Xianjun FangChi ZhaiHaixia YuYu ChenKanghui FangWan HuangXingjian ZhangZude ChangYunxin LiuXi Cao - Acute kidney injury (AKI) is marked by infiltration of immune cells, particularly macrophages and T cells, and their expansion as inflammatory and anti-inflammatory mediators to create a microenvironment critical for kidney injury/repair. As the angiotensin type 2 receptor (ATR) is emerging as reno-protective and anti-inflammatory, this study aimed to analyze the phenotypes of macrophages and helper T cells (CD4) in response to ATR activation in ischemia-reperfusion (IR)-induced AKI. - Source: PubMed
Publication date: 2026/04/02
Ali RiyasatFaisal TahmidKulkarni KalyaniPatel SanketHussain Tahir