Cynomolgus B7-2 / CD86 Protein
- Known as:
- Cynomolgus B7-2 / CD86 Protein
- Catalog number:
- CD6-C52H5
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Cynomolgus B7-2 / CD86 Protein
Related genes to: Cynomolgus B7-2 / CD86 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: Cynomolgus B7-2 / CD86 Protein
Related articles to: Cynomolgus B7-2 / CD86 Protein
- Sulforaphane (SFN), a bioactive isothiocyanate found in cruciferous vegetables, has gained considerable interest for its anti-inflammatory and immunomodulatory properties. Previous work in our lab demonstrated that tert-butylhydroquinone (tBHQ), a common food preservative and synthetic antioxidant, suppresses early T cell activation events, including production of interleukin-2 (IL-2) and other cytokines, cell proliferation and induction of interleukin-2 receptor alpha (CD25) and other inducible cell surface receptors. Based on these findings, the current study explores the effects of sulforaphane (SFN), a naturally-occurring antioxidant, on Jurkat T cell activation. Considering that sulforaphane exists as multiple isomers - the functional implications of which on T cells is unclear, we investigated the individual effects of SFN isomers on CD4 Jurkat T cell activation. Jurkat T cells were treated with 1, 3, 5, 10, 15, and 20 µM of either L-SFN or DL-SFN, following activation with anti-CD3/anti-CD28 for 24 h. Cell stimulation was assessed by measuring induction of activation markers using flow cytometry, and IL-2 cytokine secretion by ELISA. SFN inhibited upregulation of CD25, CD69, CD86, OX40 ligand (CD134) and CD40L (CD154) in a concentration-dependent manner. Likewise, SFN decreased induction of IL-2 secretion. Notably, both SFN isomers exhibited comparable suppressive effects on T cell activation. Taken together, these findings indicate that SFN suppresses induction of IL-2 and cell surface receptors in response to T cell stimulation, with no notable differences between isomers. These findings underscore the immunomodulatory properties of the dietary supplement SFN and specifically demonstrate inhibitory effects on T cell activation. - Source: PubMed
Publication date: 2026/05/18
Fu QiGardner Elizabeth MRockwell Cheryl E - Immune-related inflammation is linked to preeclampsia (PE), but immune cell-PE associations remain inconsistent. This study used two-sample Mendelian randomization (MR) to explore causal links between immune cell profiles and PE, informing clinical research and interventions. Genome-wide association study data included 731 immune cell phenotypes (3757 Europeans) and PE (2355 cases/264,887 controls, European descent). Single nucleotide polymorphisms were selected as instrumental variables (IVs) after quality control. Multiple MR methods (inverse variance weighted, weighted median estimator, weighted mode, and MR-Egger) and sensitivity analyses (heterogeneity, leave-one-out, and pleiotropy) were applied; false discovery rate (FDR) correction adjusted for multiple comparisons. Bidirectional MR explored reverse causality. After FDR correction (P_FDR < 0.20), 6 immunophenotypes showed significant causal associations with PE: 3 protective (CD62L-CD86+ myeloid dendritic cell [DC], CD62L- myeloid DC, granulocyte SSC-A levels) and 3 risk-increasing (CD16 on CD14+CD16+ monocytes, human leukocyte antigens DR+ natural killer cells, programmed death-ligand 1 on CD14-CD16+ monocytes). No horizontal pleiotropy was detected, and results were robust. Reverse MR identified 18 suggestive immunophenotypes (P < 5 × 10-6) potentially affected by PE (predominantly B cells) but no reverse causality for the 6 key phenotypes. Six immune cell phenotypes have causal links to PE, highlighting monocytes, myeloid DCs, natural killer cells, and granulocytes in PE pathogenesis. These findings offer potential immune biomarkers and therapeutic targets, emphasizing the need for translational research to validate clinical utility. - Source: PubMed
Ma LiYao LingyuJiang Mengyao - 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