CD86 FITC
- Known as:
- CD86 fluorecein
- Catalog number:
- ANT-285
- Product Quantity:
- 500µg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- CD86 FITC
Related genes to: CD86 FITC
- 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 FITC
Related articles to: CD86 FITC
- Hericium erinaceus polysaccharides (HEPs) exhibit remarkable immunomodulatory properties but are hampered by poor oral bioavailability. To overcome these limitations, this study developed and optimized HEP-loaded polyethyleneimine (PEI)-modified poly(lactic-co-glycolic acid) (PLGA) nanoparticles (HEP-PPNPs) as a novel drug delivery system. - Source: PubMed
Publication date: 2026/04/26
Zhao Yong-MingWang MaiZhang Xin-YanWang JinWang Yin-Yue - Avian influenza virus primarily invades the respiratory mucosa, necessitating the establishment of a robust mucosal secretory IgA (sIgA) barrier. However, the efficacy of avian mucosal vaccines is often hindered by inefficient antigen uptake and immune tolerance. Consequently, modern vaccine strategies focus on active targeting delivery, immune microenvironment remodeling, and activation of multifaceted immune responses. The immunogenicity and molecular mechanisms of a novel Salmonella-delivered self-amplifying RNA (saRNA) vector platform were evaluated in this study. This platform integrates bacterial surface display of a dendritic cell (DC)-targeting nanobody (Nb-phage54 via LppOmpA) with co-expression of molecular adjuvants against H9N2 influenza. The expression of HA1 and NA antigens from recombinant plasmids (pYL673, pYL679, and pYL681) was confirmed using confocal microscopy and Western blot analysis. In vitro assays revealed that the Nb-mediated targeting strain (S673) significantly increased invasion efficiency into bone marrow-derived dendritic cells and up-regulated the transcription of CCL5, CCR7, CD83, and CD86, effectively promoting DC maturation. Transcriptomic analysis (RNA-seq) revealed divergent mechanisms among vaccine candidates. The non-targeting group (S615) primarily activated antiviral innate pathways, such as JAK-STAT, whereas the targeting group (S673) significantly improved antigen processing, presentation, and natural killer cell-mediated cytotoxicity. Moreover, the adjuvant-integrated groups, S679 (CpG) and S681 (FliC), specifically triggered Toll-like receptor-21 (TLR21) and TLR5 signaling cascades by increasing cell adhesion, phagocytosis, and transmembrane signal transduction. Animal trials revealed that the targeted adjuvant vectors (S679 and S681) significantly elevated serum IgG and intestinal mucosal sIgA titers in chickens. The S679 group excelled in stimulating lymphocyte proliferation and secreting interferon-gamma and interleukin-4, indicating a potent Th1/Th2 balanced response. Challenge experiments with H9N2 virus confirmed that S679 and S681 effectively mitigated weight loss, shortened the viral shedding window, reduced viral loads in the lungs and trachea, and significantly alleviated respiratory pathological damage and inflammation. The DC-targeting saRNA-Salmonella vector developed in this study, particularly when synergized with CpG or FliC adjuvants, induced robust systemic, mucosal, and cellular immunity by activating specific intracellular signaling cascades. These findings demonstrate that this platform is a highly effective and promising candidate strategy for preventing and controlling H9N2 avian influenza. - Source: PubMed
Publication date: 2026/04/24
Wang MingyueGao YupengZhang YuxiYang TianruiZhang YuhangSun YanGuo QiyuZhang GeruiGong JinshuoWang ZhannanWang ChunfengJiang Yanlong - Regulatory T (Treg) cells that recognize dietary- or microbiota-derived antigens express RORγt and are essential for immune tolerance in the intestine. A recent paradigm shift found these cells require major histocompatibility complex class II (MHCII) on RORγt+ antigen-presenting cells (APCs) rather than conventional dendritic cells (cDCs) for signal one. Here, we evaluate signal two and unexpectedly find that costimulatory molecules B7-1 (CD80) and B7-2 (CD86) antagonize the generation of microbiota-specific RORγt+ Treg cells. Gain-of-function or loss-of-function therapeutics targeting B7 via CTLA-4 exert reciprocal effects on the generation of microbiota-specific RORγt+ Treg cells. This axis was independent of B7 on RORγt+ APCs but required MHCII on this cell type. Finally, CTLA4-Ig treatment restores microbiota-specific RORγt+ Treg cell generation and protects from experimental intestinal inflammation induced by pathobiont colonization with IL-10R signaling blockade. These results define that RORγt+ Treg cells are uniquely restrained by B7 costimulation, while CTLA4-Ig enhances immune tolerance in the intestine when acting cooperatively with RORγt+ APCs. - Source: PubMed
Publication date: 2026/04/24
Lyu MengzeSonnenberg Gregory F - Gut microbiota may affect the development of autoimmune (type 1) diabetes by differential potency of intestinal species to induce endotoxin tolerance (ET). However, where ET impinges on immune mechanisms underlying autoimmune diabetes is yet incompletely understood. We investigated the effects of lipopolysaccharide (LPS) from E. coli and B. vulgatus, two common intestinal species dominating either in low- or high-incidence countries, on activation and chemoattraction of islet-specific T cells in non-obese diabetic (NOD) mice. Intraperitoneal (i.p.) injection of E. coli LPS induced costimulatory ligands CD40, CD80 and CD86 on both conventional and cross-presenting (XCR1+) dendritic cells (DC) and islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP)-reactive islet-specific T cells in the pancreatic lymph node. In comparison to mice not primed with E. coli LPS or primed with B. vulgatus LPS, the second injection of E. coli LPS lowered the frequency of IGRP-reactive T cells and CD80 expression on DC subsets, as well as CD44 and CD69 activation markers and the CXCR3 chemokine receptor on IGRP-reactive T cells. In islets, expression of chemokine CXCL10 accentuated, and insulitis became more severe in mice primed with B. vulgatus LPS. Our results provide mechanistic insight into how ET affects islet autoimmunity and suggest that physiological exposure to E. coli LPS may benefit in moderating autoimmune diabetes. - Source: PubMed
Silojärvi Satu MLeino Linda A APöysti Sakari AHänninen Arno L M - Repetitive low-level blast exposures in rats induce the development of a post-traumatic stress disorder (PTSD)-like phenotype and evolving chronic brain vascular alterations. These alterations included atherogenic-like lesions characterized by increased extravasation of blood elements into the arterial subendothelial layers, nuclear expression of c-Fos in endothelial and vascular smooth muscle cells, vascular hyperplasia, foam cell formation, and ultimately vascular rupture. Foam cells were mainly of macrophage/microglial or of vascular smooth muscle cell origin with upregulated expression of MHC II and of its co-stimulatory molecule CD86, which is characteristic of antigen-presenting cells. Foam cells also upregulated the lysosomal CD68 marker, indicating macrophage/microglial phagocytic and inflammatory activity. Foam cells of vascular smooth muscle cell origin were present at arteriolar bends, kinks, and bifurcations and were associated with a progressive arterial network degeneration in regions with enlarged perivascular spaces. Foam cell inclusions also contained the gelatinase MMP-9, which is involved in extracellular matrix degradation, and the pro-inflammatory cytokine TNF-α that further induces foam cell formation. These findings indicate that the chronic atherogenic lesions associated with blast-induced vascular degeneration may trigger a progressive pro-inflammatory state and expand the progressive vascular degeneration associated with the PTSD-like phenotype. - Source: PubMed
Publication date: 2026/04/23
Gama Sosa Miguel ADe Gasperi RitaLind Rachel HPryor DylanPerez Gissel MPerez Garcia Georgina SAbutarboush RaniaKawoos UsmahZhu Carolyn WJanssen William G MHof Patrick RAhlers Stephen TElder Gregory A