Rat Anti-Mouse CD80
- Known as:
- Rat Antibody toMouse CD80
- Catalog number:
- 128-10053-1
- Product Quantity:
- 500
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rat Anti-Mouse CD80
Related genes to: Rat Anti-Mouse CD80
- Gene:
- CD80 NIH gene
- Name:
- CD80 molecule
- Previous symbol:
- CD28LG, CD28LG1
- Synonyms:
- B7.1, B7-1
- Chromosome:
- 3q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-14
- Date modifiied:
- 2016-10-05
Related products to: Rat Anti-Mouse CD80
Related articles to: Rat Anti-Mouse CD80
- Thiazolidine derivatives exert anti-inflammatory effects by inhibiting the NF-κB pathway and promoting macrophage polarization toward the anti-inflammatory M2 phenotype, partially through PPARγ activation. Our previous work identified thiazolidine derivative 13 [methyl 2-(benzoylimino)-3-methyl-4-(4-nitrobenzyl)-1,3-thiazolidine-4-carboxylate] as a potent immunomodulator that reduces pro-inflammatory mediators and enhances anti-inflammatory markers. However, its direct interaction with PPARγ remains unclear. This study aims to evaluate whether thiazolidine 13 activates PPARγ and contributes to M2 macrophage polarization using LPS-stimulated RAW 264.7 cells, cell transactivation assay and reporter gene (Hella cells), LPS-stimulated THP-1 cells, and molecular docking analysis. Compound 13 reduced NO₂⁻ production, CD80 expression, and pro-inflammatory cytokines while increasing IL-10, TGF-β, and CD206 in LPS-stimulated RAW 264.7 macrophages. Compound 13 also inhibited NO production in LPS-stimulated THP-1 cells. These effects were only partially reversed by PPARγ antagonists, suggesting additional PPARγ-independent mechanisms, while the induction of CD206 was closely linked to partial PPARγ activation. Docking studies supported this profile, showing that the (S) enantiomer of thiazolidine 13 adopts a binding mode typical of partial PPARγ agonists and exhibits a higher predicted affinity than the (R) enantiomer. Compound 13 acts as a partial PPARγ modulator capable of shifting macrophages from a pro-inflammatory toward an anti-inflammatory phenotype (M2-like). This dual action relies on the inhibition of NF-κB signaling and partial PPARγ activation. The predominance of the M2-like subpopulation, underscores its role in resolving inflammation and promoting tissue repair. - Source: PubMed
Publication date: 2026/04/22
Mohr Eduarda Talita BramorskiLubschinski Tainá LarissaMoro Pedro Augusto MaroccoBenvenutti LarissaCosta Natáli Tereza Capistranode Sousa Pedro Luís Pereira BragaSá Marcus MandolesiHernandes Marcelo ZaldiniMilton Flora AparecidaSantin José RobertoDalmarco Eduardo Monguilhott - 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 - Peritoneal cavity (PerC) B cells can be classified into distinct subpopulations; however, their differential antigen-presenting capabilities and roles in antitumor immune responses remain largely unexplored. This study aimed to elucidate the properties of PerC B cell subpopulations in antitumor immune responses by using ovalbumin (OVA) peptides as neoantigen mimics and employing OT-I mice, which express a transgenic T cell receptor specific to OVA peptides. We found that OVA-pulsed PerC B cells effectively stimulated CD8+ T cell proliferation, although their antigen-presenting capacity was lower than that of splenic B cells. Subpopulation analysis revealed that CD11b+CD80+ and CD11b-CD80+ B cells produced high levels of interleukin 10 (IL-10), contributing to immunosuppressive effects. Blocking IL-10 significantly enhanced T cell proliferation and cytotoxicity, whereas PD-L1/PD-L2 blockade had no significant impact. The CD8+ T cell response in OT-I mice, stimulated by bone marrow-derived dendritic cells (BMDCs) that had phagocytosed OVA, was dose-dependently suppressed by OVA-pulsed peritoneal B cells. In an in vivo tumor model using Rag2-/- mice, co-administration of OVA-pulsed PerC B cells transiently suppressed tumor growth at lower B: T ratios but promoted tumor progression at higher B: T ratios. IL-10 knockdown in PerC B cells further enhanced tumor suppression. These findings suggest that PerC B cells exhibit a dual role in antitumor immunity, modulating CD8+ T cell responses in a density-dependent manner. While they can function as antigen-presenting cells to enhance T cell activation, their IL-10-mediated immunosuppressive properties can dampen antitumor responses. Understanding this balance may provide insights for optimizing B cell-based immunotherapies. - Source: PubMed
Mochizuki TetsuyaTanaka YukaIde RyutaOhdan Hideki - Rheumatoid arthritis (RA) is an autoimmune disorder characterized by chronic joint inflammation. Although sinomenine (SIN) is clinically effective against RA, its potential to modulate autoantigen-specific immune responses and the underlying mechanisms remain incompletely understood. - Source: PubMed
Publication date: 2026/04/16
Zhang DingdingWu LishengChen FeilongChen XiaoyunZheng SongyuanLi JuanChen Shixian - Neuromyelitis optica spectrum disorders (NMOSD) are an immune-mediated inflammatory disease of the central nervous system (CNS) primarily characterized by anti-aquaporin-4 immunoglobulin G (AQP4-IgG)-mediated astrocyte injury, neuroinflammation, and demyelination. However, the relationship between the disease and the immune trait from a genetic perspective still requires further confirmation. - Source: PubMed
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