Ask about this productRelated genes to: CD80 antibody
- 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: CD80 antibody
Related articles to: CD80 antibody
- This study investigates METTL3's function and mechanisms in hemorrhoidal disease-related inflammation. - Source: PubMed
Publication date: 2026/05/21
Li ChunlingHan XuChen AiliCheng JianLi YalongWang QiongZhang Heng - Intracerebral hemorrhage (ICH) is a clinically prevalent cerebrovascular disorder in which neuroinflammation is a major contributor to secondary brain injury. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key regulator of intracellular redox homeostasis, whereas apoptosis signal-regulating kinase 1 (ASK1) is involved in stress-associated inflammatory and apoptotic signaling. However, the relationship between Nrf2 signaling and ASK1/JNK pathway activity in ICH-related inflammatory injury remains incompletely understood. In this study, we established a rat ICH model and used molecular, histological, and behavioral approaches to examine the association between Nrf2 signaling and ASK1/JNK-related neuroinflammatory changes. We found that ICH was accompanied by increased Nrf2 and phosphorylated ASK1 expression. siRNA-mediated modulation of Nrf2 or ASK1 was associated with reciprocal changes in ASK1/JNK pathway activation. In parallel, changes in CD80/CD206 expression and inflammatory cytokine levels suggested that Nrf2 signaling was associated with altered inflammation-related responses, potentially involving ASK1/JNK pathway activity. Histological analyses, including TUNEL staining, Nissl staining, and brain water content measurement, further showed that preservation of Nrf2 signaling was associated with reduced neuronal injury and cerebral edema after ICH. Behavioral assessments showed corresponding changes in locomotor and anxiety-related performance. Overall, these findings support an association between Nrf2 signaling and ASK1/JNK-related neuroinflammatory responses following ICH and provide a basis for further mechanistic investigation of this pathway in hemorrhagic brain injury. - Source: PubMed
Publication date: 2026/05/20
Gu YutingYuan HuaZhao GuangChen YuyangGuo ZhiqiangZeng MeiFeng QiupengZhou PingChen ZheLiu HuaXia Xiaohua - In enzootic bovine leukosis (EBL), a B-cell lymphoma caused by bovine leukemia virus (BLV) infection, immune remodeling within tumor-affected lymph nodes is currently poorly understood. Here, we analyzed chemokine production and macrophage phenotypes in tumor-affected lymph nodes in EBL, focusing on CCL4. Intracellular cytokine staining revealed that, compared with healthy lymph nodes, EBL tumor-affected lymph nodes showed increased proportions of CCL4 expressing cells, particularly among CD4 T cells and B cells. Functional migration assays showed that recombinant CCL4 induced robust monocyte migration, with a comparatively modest T-cell migration. To identify lymph node macrophages, we characterized CD11bCD172a cells and confirmed their macrophage identity based on high expression levels of CD11c, CD14, CD16, and CD68. Using this definition, we found that the CD11bCD172a population was markedly increased in tumor-affected lymph nodes. Phenotypic analysis revealed an increased proportion of CD163 and CD163PD-L1 macrophages, consistent with the acquisition of an immunosuppressive phenotype. In parallel, macrophages in tumor-affected lymph nodes showed a shift from MHC class I/II to MHC I/II subsets and reduced co-expression of MHC molecules with CD80 and CD86, indicating impaired antigen-presenting features. Collectively, these findings suggest that elevated CCL4 production in tumor lesions induced by EBL is associated with monocyte recruitment and the accumulation of phenotypically altered macrophages, highlighting a chemokine-driven remodeling of the tumor immune microenvironment. - Source: PubMed
Publication date: 2026/05/04
Nakamura HayatoOkagawa TomohiroHamaïdia MalikTiyamanee WisaIkehata MariHirose MinagiInoue MahoWillems LucMaezono KeisukeThammahakin PassawatKobayashi ShintaroKato YukinariSuzuki YasuhikoMaekawa NaoyaMurata ShiroOhashi KazuhikoKonnai Satoru - Dendritic cells (DCs) play a pivotal role in initiating robust T cell responses against tumors, yet effective strategies to enhance DC activation remain limited. This study explores the synergistic effects of Lycium barbarum polysaccharide (LBP) and the tumor cell lysate of endothelial progenitor cells (EPC-TCL) to boost DC activation and anti-tumor immunity. Using flow cytometry, the enzyme-linked immunosorbent assay, western blot analysis, and in vivo tumor models, we demonstrate that the combination treatment significantly enhanced expression of co-stimulatory molecules (CD40, CD80, CD86, and MHC-I) in DCs and elevated cytokine levels (IL-6 and IL-12). Co-culture experiments revealed that T cells primed with LBP and EPC-TCL-modified DCs increased proliferation and reduced exhaustion, characterized by upregulated CD69 and downregulated PD-1. Mechanistically, activation of the MAPK and STING signaling pathways was confirmed by phosphorylation of key proteins. Moreover, T cells activated by DCs treated with LBP and EPC-TCL exhibited potent anti-tumor effects, significantly reducing invasiveness of mouse lung carcinoma cells and impairing angiogenesis in vitro. In a mouse axillary tumor model, the combination treatment markedly suppressed tumor growth and induced apoptosis of tumor cells. These findings highlight the potential of LBP and EPC-TCL as novel immunotherapeutic agents targeting DCs to enhance anti-tumor immunity. Future studies will focus on clinical validation and integration into combination therapies for broader cancer applications. - Source: PubMed
Publication date: 2026/05/19
Wang LifangWang ZiyeZhu ChangchangChen WenhuZhao Hongguang - Identifying autoantigens in multiple sclerosis (MS) has been challenging. If successful, this could facilitate development of autoantigen-specific tolerogenic therapies, by exposing antigen presenting cells (APC) to tolerogenic stimuli with autoantigens specific to the human leukocyte antigen (HLA) haplotype of patients. RAS guanyl releasing protein 2 (RASGRP2), which is expressed by lymphocytes and striatal neurons, is a putative autoantigen in HLA-DRB1*15:01 (DR15)-positive individuals. We aimed to identify antigenic RASGRP2 epitope(s) that could be used to develop tolerogenic therapies. RASGRP2-derived peptides of varying DR15 binding affinities were exposed to peripheral blood mononuclear cells (PBMCs). Immunoeptidomic techniques demonstrated strong and moderate binding affinity RASGRP2 peptides could be presented by HLA-DR on PBMCs from DR15-homozygous or DR15-negative patients. Moderate affinity peptides produced the greatest increase in CD80 expression and pro-inflammatory cytokine (IFN-γ, IL-17, IL-22) secretion by PBMCs, particularly in DR15-positive patients. One RASGRP2 peptide eliciting the highest pro-inflammatory responses was used to generate HLA-DR15 tetramers. CD4+ T-cells specific for this peptide were four-fold higher in frequency in DR15-positive patients versus controls, more pro-inflammatory in phenotype and demonstrated increased peptide-stimulated proliferation. In conclusion, we identified a novel immunogenic RASGRP2 peptide with relative selectivity for HLA-DR15-positive people with MS, which could form the basis for autoantigen-specific tolerogenic therapy. - Source: PubMed
Publication date: 2026/05/15
Li VivienPandey KirtiBinder Michele DReid Hugh HLim Jia JiaLoh Tiing JenTran Mai TRossjohn JamiePurcell Anthony WKilpatrick Trevor J