Anti_Human, mab CD80 Source Mouse
- Known as:
- Anti_Human, mab CD80 Source Mouse
- Catalog number:
- 101-M315
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Human mab CD80 Source Mouse
Related genes to: Anti_Human, mab CD80 Source Mouse
- 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: Anti_Human, mab CD80 Source Mouse
Related articles to: Anti_Human, mab CD80 Source Mouse
- Immunodeficiency represents a burgeoning health concern, and modulating the immune response dietary intervention is regarded as a novel strategy to improve immune function. In this research, rice bran peptides (RBPs) were prepared enzymatic hydrolysis combined with fermentation by . Compositional analysis revealed that the soluble protein content of RBPs increased from 6.73% to 74.24%, and the peptide fraction with a molecular weight less than 1.0 kDa increased from 0.67% to 6.92%. RBPs had no impact on the viability of RAW264.7 cells; however, they significantly elevated the phagocytosis rate of RAW264.7 cells ( < 0.01). Morphological examination demonstrated that RBPs could alter the cell morphology. Flow cytometry indicated that the expression of CD80 and CD86 on the surface of RAW264.7 cells was upregulated after treatment with RBPs. The DCFH-DA probe assay showed that RBPs could enhance the production of reactive oxygen species (ROS) in RAW264.7 cells. RBPs significantly enhanced the activity of acid phosphatase (ACP) in RAW264.7 cells ( < 0.01). They also facilitated the secretion of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10), and significantly increased the content of toll-like receptor 4 (TLR4). These findings suggest that RBPs have the potential to serve as a natural food-derived immunomodulatory factor. - Source: PubMed
Publication date: 2026/05/26
Lin WeiSui XinlaiLiu XiaolanZheng Xiqun - Highly accessible genomic super-enhancers often drive tumor-promoting programs, yet the impact of genomic variation within these regulatory elements remains unclear. Here, we identified a bifunctional super-enhancer that regulates the expression of cancer-promoting genes LINC00636 and CD47 in breast cancer. We discovered that a common germline insertion variant within the super-enhancer is associated with reduced chromatin accessibility at the super-enhancer locus. Deletion of the insertion in breast cancer cells increased chromatin accessibility, leading to upregulation of LINC00636 and CD47, enhanced resistance to nutrient-deprivation-induced apoptosis (mediated by CD47), activation of senescence (driven by elevated LINC00636), delayed cell death, and reduced infiltration of CD80⁺ pro-inflammatory macrophages, changes that represent tumor-promoting features. Together, our findings uncover a common insertion-deletion variant that fine-tunes the regulatory activity of a bifunctional super-enhancer, suggest a protective role for the insertion allele, and establish a previously unrecognized role for LINC00636 in senescence and breast cancer biology. - Source: PubMed
Publication date: 2026/05/12
Dibenedetto CarolinaTsark AmeliaAcenas DanizaThach AlysiaSinghal AnmolOpazo-Mellado ValentinaLemus Anthony RodriguezZeini Mustapha ElZhang HuiPark CatherineVelozo Hugo GonzalezWeissmann IrvingBetancur Paola - Long-Lived Plasma Cells (LLPCs) are an integral part of long-term protective humoral immunity. They can live for decades, unlike Short-Lived Plasma Cells (SLPCs), and continuously produce antibody regardless of antigen stimulation, unlike Memory B Cells (MBCs). LLPCs are critical for the sustained protective immunity against pathogens that are only intermittently present in a population but can cause significant morbidity/mortality when active-such as epidemic diseases. What drives B cell differentiation specifically to the LLPC lineage is still not fully understood; there is conflicting information on what drives the fate decisions for MBCs vs. SLPCs vs. LLPCs. Evidence suggests that although LLPC and SLPC have similar gene transcriptional profiles they differ significantly in their metabolic profiles-likely due to the demands of prolonged continuous antibody production in LLPC. These metabolic changes include increased uptake of metabolic substrates, increased mitochondrial mass/function and enhanced fuel availability via lipophagy, and enhanced proteostasis to remove misfolded proteins. However, the possibility of repeated antigen-driven generation of a large number of highly metabolically active long-lived cells is problematic for a resource-constrained organism, and it is now clear that LLPC numbers are constrained by a limited number of specialized LLPC niches in the bone marrow and other tissues. LLPCs are not intrinsically long-lived but rely on interactions with the LLPC niche to maintain their longevity. For example, activation of the CD28 receptor on LLPC by its ligands CD80/CD86 on dendritic cells (DC) in the LLPC niche results in augmented metabolism through enhanced lipophagy, intracellular long chain fatty acid availability, oxidative phosphorylation, increased mitochondrial mass and function that are necessary for LLPC survival. CD28 activation is essential for the survival of LLPC but not for SLPC, supporting the concept that enhancement of LLPC metabolic capacity by interactions with its niche plays a key role in LLPC longevity. In human health, new insights into how LLPCs survive and differentiate will impact the development of robust and long-lasting vaccinations, as well as with treatment of autoantibody-mediate autoimmune diseases and PC malignancies such as multiple myeloma (MM)-as these malignancies remain dependent on many of the same survival pathways as their nonmalignant LLPC counterparts. - Source: PubMed
Publication date: 2026/05/07
Reinke Julia GraceSchorr ChristopherLee Kelvin Paul - Technology that precisely controls macrophage polarization to distinct functional states would deepen our understanding of macrophage biology and enable the development of new macrophage cell therapies. Here, we use a synthetic cytokine receptor (SCR) platform with a programmable signaling domain to control the polarization of primary human macrophages. SCRs containing signaling motifs from the interferon-gamma (IFN-γ) or Interleukin-10 (IL-10) receptors mimic key features of pro-inflammatory or anti-inflammatory polarization, respectively. Random recombination of nine distinct signaling motifs to create new SCR signaling domains generates a diverse landscape of synthetic macrophage states with varied expression of inflammatory markers (CD80, CD40) and anti-inflammatory markers (CD163, CD206), and varied phagocytic capacity. SCRs programmed with multiple YLxQ motifs increase macrophage phagocytosis of and chimeric antigen receptor (CAR)-macrophage phagocytosis of cancer cells in mice, reducing tumor burden by 30-fold. The motif-dependent polarization is well-described by a two-state model, enabling quantitative prediction of macrophage polarization state from SCR signaling domain composition. Leveraging this model, we design an SCR that simultaneously enhances phagocytosis and maintains a macrophage pro-inflammatory state. Together, these findings establish a framework for synthetic programming of macrophage polarization states, with potential applications in cancer immunotherapy and other disease contexts. - Source: PubMed
Publication date: 2026/05/14
Lunger Judith CSant'Anna Lucas ESalcido-Alcántar AntonioArroyo Hornero RebecaCho WansangVaughan-Jackson AlunGu MingxinLiu Jenny YBeckett Alex NParrilla-Garcia JoaquinRamakrishna SnehaBassik Michael CDaniels Kyle G - Retrospective studies in patients with non-muscle invasive bladder cancer (NMIBC) have reported a significant reduction in Alzheimer's disease (AD) incidence (12-78%) among Bacillus Calmette-Guérin (BCG) recipients versus controls. To investigate the underlying mechanisms, we evaluated BCG in the PS19 mouse model of tauopathy. We found that BCG administration reduced hippocampal phospho-tau and microgliosis while preserving neuronal markers. volumetric T2-MRI demonstrated attenuation of brain atrophy accompanied by increased glutamate-weighted CEST-MRI signals. Functionally, BCG-treated mice showed improved performance in the novel object recognition test (NORT), as well as improved body-weight maintenance and survival. Transcriptomic profiling of the hippocampus revealed near complete normalization of the PS19 disease-associated gene expression signature towards that of healthy controls. Flow cytometric profiling of brain myeloid populations demonstrated a reduction in activated resident microglia, but total microglia cells remain elevated. Moreover, an increase of the co-stimulatory marker CD80 on the recruited peripheral myeloid cells ensues following BCG treatment. Consistent with this shift in myeloid state, primary brain myeloid cells from BCG-treated mice also exhibited enhanced phagocytosis of FITC-labeled tau fibrils and increased lactate production. Together, these findings indicate that BCG induces systemic and CNS myeloid cell reprogramming that limits neuroinflammation, enhances tau clearance, and rescues cognitive and neurodegenerative phenotypes in a tauopathy model. BCG is a safe, readily available therapy that merits consideration as a preventive agent against dementia. - Source: PubMed
Publication date: 2026/05/15
Shee SomnathHuang MeixiangBaghel Meghraj SinghZheng YuxinLun ShichunYadav Santosh KYadav Nirbhay NRuiz-Gonzalez Carlos ETyagi SandeepNuermberger EricJain Sanjay KBhujwalla Zaver MSlusher Barbara SWong Philip CBishai William