CD80
- Known as:
- CD80
- Catalog number:
- 11-287-C025
- Product Quantity:
- 0.025 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD80
Related genes to: 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: CD80
Activation B7-1 antigen,B7,B7,Cd80,Mouse,Mus musculus,T-lymphocyte activation antigen CD80Activation B7-1 antigen,B7,BB1,CD28LG,CD28LG1,CD80,CTLA-4 counter-receptor B7.1,Homo sapiens,Human,LAB7,T-lymphocyte activation antigen CD80Activation B7-1 antigen,CD80,Oryctolagus cuniculus,Rabbit,T-lymphocyte activation antigen CD80anti-CD80anti-CD80anti-CD80anti-CD80anti-CD80anti-CD80 (1G1)anti-CD80 (3D7)anti-CD80 (3E10)anti-CD80 (4A4)anti-CD80 (1G1)anti-CD80 (1G1) type: Primary antibodies host: Mouseanti-CD80 (2A2) Related articles to: CD80
- The generation and maintenance of effective tumor-specific CTL responses require more than antigen recognition. In most settings, TCR engagement must be accompanied by co-stimulatory input, with the B7-1/B7-2-CD28 axis being one of the best-characterized examples. When this second signal is weak or absent, tumor-reactive CD8+ T cells may recognize tumor antigens but fail to expand, survive, or acquire and sustain cytotoxic activity. Tumors take advantage of this vulnerability by reducing co-stimulatory ligand availability, increasing inhibitory checkpoint signaling, and remodeling the tumor microenvironment in ways that further restrict T-cell activation. Depending on the stage and context of dysfunction, this shift may favor anergy-like dysfunction, impaired persistence and apoptotic attrition, or, under persistent antigen exposure and sustained inhibitory signaling, exhaustion-associated dysfunction, thereby promoting immune escape. This review examines how reduced or functionally restricted B7-CD28 co-stimulation impairs CTL activation, intratumoral reactivation, and persistence, and how checkpoint signaling, suppressive immune cells, metabolic stress, and stromal barriers compound this defect within tumors. We also evaluate strategies intended to restore or bypass inadequate co-stimulatory input, distinguishing established checkpoint-based interventions from co-stimulatory agonists, engineered T-cell therapies, multispecific antibodies, and gene-based approaches that remain preclinical or early translational in many settings. We propose that mechanism-matched therapy should be guided by the phase at which the dominant barrier arises-tumor-reactive CD8+ T-cell priming, intratumoral CTL reactivation, or long-term CTL persistence. - Source: PubMed
Publication date: 2026/07/28
Ma JunjieChen JingMiao TianrunLi YehongLi YongmengZhao LeiTian Hui - As a prevalent malignancy, liver cancer ranks as the third most common cause of cancer mortality globally. Within the tumor microenvironment, tumor-associated macrophages (TAMs) exhibit contrasting functional phenotypes: the anti-tumor M1 type and the pro-tumor M2 type. Reprogramming TAMs from the M2 to the M1 phenotype has emerged as a promising immunotherapeutic strategy. Here, we engineered a multi-nano therapeutic system, PAH@HMMDN@R848, by loading a TLR7/8 agonist (R848) onto hollow MnO2 nanoparticles (HMMDN) and coating with polyallylamine hydrochloride (PAH). In vitro, this system efficiently repolarized M2 macrophages to the M1 phenotype, evidenced by decreased CD206, Arg-1, IL-10 and increased CD80, iNOS, TNF-α (P < 0.05). Under acidic/glutathione-rich conditions, HMMDN degraded to release Mn2+, which served as a T1-weighted MRI contrast agent with a high relaxivity (r1 = 5.255 mM-1 s -1). Mechanistically, PAH@HMMDN@R848 activated both NF-κB (via R848) and STING (via Mn2+) pathways, leading to synergistic M1 polarization. In a subcutaneous H22 liver cancer mouse model, intratumoral injection of PAH@HMMDN@R848 significantly suppressed tumor growth (tumor inhibition rate 80.6%) without obvious systemic toxicity. Immunohistochemistry and cytokine analysis revealed that the treatment increased M1 macrophage infiltration (CD80+) and reduced M2 macrophages (CD206+) within tumors, along with elevated TNF-α/iNOS and decreased IL-10/Arg-1. This study presents a multifunctional nanoplatform capable of TAMs reprogramming and MRI diagnosis, offering a promising approach for liver cancer theranostics. - Source: PubMed
Publication date: 2026/09/18
He Pei-PeiHou Zheng-JuLi Han-MeiZhang Ji-XuanChen An-QiMiao Quan-YouYang Chao-FengYu Jin-HongLi Yang - Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the selective loss of motor neurons in the brain and spinal cord with evidence of local neuroinflammation. Regulatory T cells (Treg) exert neuroprotective effects and correlate with disease progression, but central mechanisms governing Treg development during ALS remain unclear. We investigated the thymic architecture and T cell differentiation in SOD1-G93A (mSOD1) ALS mice at multiple disease stages. Thymocyte and thymic epithelial cells (TEC) subpopulations, as well as stages of Treg differentiation and suppressive capacity, were analyzed by flow cytometry, immunofluorescence, and functional assays. At late disease stage (120 days-old), mSOD1 mice displayed thymic atrophy, reduced thymocyte numbers, and decreased double-positive (DP), CD4 single-positive (SP), and Treg populations. Foxp3 expression per cell was preserved, but Treg progenitors and mature Treg numbers declined, paralleled by reduced suppressive function . TEC analysis revealed reduced total and mature medullary TEC (CD80MHCII), despite preserved Aire expression. Foxp3 cells were abnormally localized at cortical sites, away from mTEC, associated with migratory abnormalities and increased apoptosis. TREC evaluation revealed reduced intrathymic sjTREC, consistent with impaired proliferation and differentiation between DN and DP stages, although peripheral sj/βTREC ratios remained stable. Reduced Treg numbers were also observed in lymph nodes draining affected hindlimbs. Our findings identify the thymus as a target organ in ALS, where thymic involution, TEC loss, and Treg dysfunction may compromise immune tolerance. These alterations likely reinforce the role of the thymus in peripheral immune dysregulation and neuroinflammation observed in ALS. - Source: PubMed
Publication date: 2026/09/06
Lemos Julia PereiraStockholm DanielDinatale BrendaChaves Amanda SilvaPezet SoniaFrias Carvalho ViniciusPérez Ana RosaMendes-da-Cruz Daniella ArêasSavino WilsonSmeriglio Piera - Tregs play an essential role in immune tolerance, and Treg-promoting therapies are in development for the treatment of many inflammatory disorders. Interleukin-2 (IL-2)-based therapies increase Treg frequency, but little is known about impacts on Treg heterogeneity and function. We extended analyses of an IL-2 mutein (MK-6194) single-ascending-dose trial in healthy human participants by comprehensively defining Treg subsets and gene expression changes in vitro and in vivo. We found highly specific and dose-dependent activation and expansion of Tregs in clinical and pre-clinical studies. Following a single subcutaneous dose in humans, thymic-derived Tregs were selectively activated and expanded, while peripherally induced Tregs were unaffected. Expanded Tregs had increased expression of genes and proteins consistent with activation, suppressor function, and homing to non-lymphoid tissue, as well as increased transendocytosis activity, as measured by CTLA-4-dependent capture of CD80 and CD86 from non-Tregs. These results shed light onto underlying mechanisms by which Treg-targeted therapy may promote immune tolerance. - Source: PubMed
Publication date: 2026/09/17
Cooney Laura AFahning MitchKhoryati LilianeKus AnnaScheiding SheilaBlanchfield LoriLawrance MatthewBenson BasilinHarris Kristina MBaltus Gretchen AAgarwal ShiuliWnek RichardScheid Johannes FCunningham-Bussel KikiKim Nancy DStoch S AubreyVisweswaraiah JyothsnaHigginson-Scott NathanKis-Toth KatalinViney Joanne LOtipoby Kevin LSampson ErikLarkin BridgetCampbell Daniel JLong S Alice - Ageing is associated with colon epithelial barrier disruption and up-regulation of myelopoiesis in the bone marrow (BM). Alamandine (Ala) and MrgD are novel members of the renin angiotensin system (RAS). This study tested the hypothesis that Ala restores the colon epithelial barrier integrity in ageing via modulating gut-BM axis. - Source: PubMed
Publication date: 2026/09/16
Chittimalli KishoreRozario Henryata EMartinez VictorMcAdams Zachary LAdkins Stephen AEricsson Aaron CJarajapu Yagna P R