Human B7-2 / CD86 Protein
- Known as:
- Human B7-2 / CD86 Protein
- Catalog number:
- CD6-H5223
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human B7-2 / CD86 Protein
Related genes to: Human 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: Human B7-2 / CD86 Protein
Related articles to: Human B7-2 / CD86 Protein
- Sepsis is characterized by dysregulated inflammatory responses triggered by pathogen-associated molecular patterns (PAMPs) and remains a major cause of mortality worldwide. Although antibiotics are widely used for the treatment of sepsis-associated infections, their clinical efficacy is often limited by antimicrobial resistance and the inability to control excessive inflammatory responses. Indolicidin is a bovine-derived antimicrobial peptide with antimicrobial and immunomodulatory activities; however, its anti-inflammatory mechanisms in sepsis remain unclear. In this study, we investigated the protective effects and mechanisms of indolicidin in bacterial and fungal sepsis models. The results showed that indolicidin exhibited good biocompatibility both in vitro and in vivo. In murine models of - and -induced sepsis, indolicidin significantly improved survival and reduced microbial burden in the kidneys. In RAW264.7 macrophages stimulated with lipopolysaccharide (LPS), a major PAMP of , indolicidin suppressed M1 polarization, reactive oxygen species production, and proinflammatory cytokine expression. Transcriptomic analyses of macrophages and infected kidney tissues revealed that indolicidin consistently downregulated inflammation-related pathways, chemokine signaling, and LPS-response pathways, including genes associated with IL-6, chemokines, and M1 macrophage markers such as CD80 and CD86. Mechanistically, indolicidin directly bound LPS, interacted with lipopolysaccharide-binding protein (LBP), and reduced the surface expression of CD14 and the TLR4/MD2 complex, indicating modulation of the TLR4 signaling pathway. Overall, this study highlights indolicidin as a dual-function peptide with antimicrobial and immunomodulatory activity and supports its potential as a therapeutic candidate against sepsis. - Source: PubMed
Publication date: 2026/06/17
Shi ZhishangWang YantingGu YijunZhu MengsenLi MingchunYu Qilin - The combination of tyrosine kinase inhibitors (TKIs) like lenvatinib with immune checkpoint inhibitors (ICIs) has become a cornerstone of first-line therapy for advanced hepatocellular carcinoma (HCC). However, this approach faces a significant bottleneck, with objective response rates lingering around 20-36%, largely due to the non-immunogenic ("cold") nature of most HCC tumors. This highlights a critical need for strategies that can remodel the tumor immune microenvironment to enhance therapeutic efficacy. - Source: PubMed
Publication date: 2026/06/16
Feng Shan-RuDong En-FuGao ZhengXu Mo-RanKwangwari PascalSun Cheng-QiangChen Jia-FengShi Ying-HongLiu Wei-RenWu Wei-XunZhang XinHuang AoLuo Xuan-MingGao QiangShi Guo-MingKe Ai-WuZhou JianFan JiaWang Xiao-YingQie Jing-BoFu Xiu-TaoDing Zhen-Bin - CS polarity, the mutually exclusive expression of CXCL9 and SPP1, is a key feature of tumor-associated macrophages (TAMs) in the lung adenocarcinoma (LUAD) microenvironment. The mechanisms and impact of CS polarity on tumor progression remain incompletely understood. The study aims to define the molecular basis of CS polarity and its role in LUAD progression to inform new immunotherapies. - Source: PubMed
Publication date: 2026/06/16
Liu HaixiaoWang LingyunLi ChanglinLi DongtaoMeng LinghanZheng GuangdaRen JuanxiaShang LuBao Yanju - Growing evidence indicates that immune and metabolic dysregulation contribute to the development of appendicitis; however, the causal pathways remain unclear. This study employed Mendelian randomization (MR) to assess the effect of immune cell traits on appendicitis risk, with an emphasis on the mediating role of plasma metabolites. We utilized publicly available summary statistics from genome-wide association studies based on European cohorts, encompassing 731 immune cell traits, 1400 plasma metabolites, and appendicitis. The inverse variance weighted method served as the primary analytical strategy. Mediation analysis was conducted to estimate indirect effects, and reverse MR was performed to evaluate reverse causality. To address multiple testing in these high-dimensional screens, Benjamini-Hochberg false discovery rate adjustment was additionally applied within the immune-cell and plasma-metabolite discovery stages. Three immune cell traits and 12 plasma metabolites were significantly associated with appendicitis. Specifically, CD86+ plasmacytoid DC %DC exhibited a protective effect (odds ratio [OR]: 0.910, P = .003), while CD28+ DN (CD4-CD8-) %T cell (OR: 1.090, P = .001) and CD27 on IgD+ CD38- unsw mem (OR: 1.071, P = .002) were associated with increased risk. Among the identified metabolites, 7 exhibited protective effects, whereas 5 were linked to elevated risk. Notably, 13-HODE + 9-HODE levels partially mediated the effect of CD28+ DN (CD4-CD8-) %T cell on appendicitis (mediation proportion: 17.7%, P < .001). No evidence of heterogeneity, horizontal pleiotropy, or reverse causation was detected in sensitivity analyses and reverse MR. However, after false discovery rate adjustment, none of the immune-cell or metabolite associations remained significant; these signals should therefore be interpreted as exploratory candidates rather than definitive findings. This study provides evidence supporting a role for the immune-metabolic axis in the pathogenesis of appendicitis, providing novel insights into causal mechanisms and informing potential strategies for targeted prevention. Accordingly, the present results are best viewed as hypothesis-generating and require validation in stratified and prospective datasets before clinical translation. - Source: PubMed
Zheng HaixiaWang KuiWang Dong - Inflammatory microenvironments regulate immune cell differentiation, activation, and programming. Although traditionally considered terminally differentiated effectors, neutrophils can acquire distinct functional states in response to environmental cues. To examine context-dependent neutrophil programming, cells from healthy donors were cultured in vitro under cytokine regimens mimicking opposing inflammatory environments (GM-CSF/IFN-γ or IL-4/IL-13/TGF-β), alone or combined with PMA and Mycobacterium tuberculosis, to assess functional and transcriptional responses. GM-CSF/IFN-γ-conditioned neutrophils exhibited increased cell size, altered nuclear morphology, enhanced MHC class II and CD86 expression, and elevated IL-8 and reactive oxygen species production. This profile was associated with increased TNF-α, IL-10, TLR2, and TLR4 gene expression and reduced global DNA methylation. In contrast, IL-4/IL-13/TGF-β-conditioned neutrophils resembled non-conditioned controls regarding surface markers and cytokine production but showed reduced ROS generation and increased DNMT3A expression. Upon in vitro infection with M. tuberculosis, GM-CSF/IFN-γ-conditioned neutrophils produced higher IL-8 and IL-1β levels and formed more neutrophil extracellular traps. Additionally, plasma from patients with severe tuberculosis modulated TLR4, CCR7, and IP-10 expression in healthy neutrophils, indicating systemic inflammatory influences. These findings demonstrate that inflammatory conditioning induces coordinated transcriptional and epigenetic remodeling, shaping neutrophil antimicrobial and immunoregulatory potential in infectious contexts. - Source: PubMed
Publication date: 2026/06/13
Almeida Cicero José Luíz Dos RamosCastro Ricardo CardosoCardoso-Silva Priscilla MarianeZambuzi Fabiana AlbaniSilva Patrick FernandesBrauer Veronica SoaresGravina Humberto DorigettoFontanari CarolineBollela Valdes RobertoFrantz Fabiani Gai