Anti-Mouse_Rat Foxp3 PE 25 ug
- Known as:
- Antibody toMouse_Rat Foxp3 PE 25 ug
- Catalog number:
- 12-5773-80
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse_Rat Foxp3 25
Related genes to: Anti-Mouse_Rat Foxp3 PE 25 ug
- Gene:
- FOXP3 NIH gene
- Name:
- forkhead box P3
- Previous symbol:
- IPEX
- Synonyms:
- JM2, XPID, AIID, PIDX, DIETER, SCURFIN
- Chromosome:
- Xp11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-05
- Date modifiied:
- 2019-04-23
Related products to: Anti-Mouse_Rat Foxp3 PE 25 ug
Related articles to: Anti-Mouse_Rat Foxp3 PE 25 ug
- Various studies have reported aberrant function of the immune system in endometriosis. This highly prevalent disease can initiate and progress by numerous genetic and epigenetic alterations that affect immune system functions. Regulatory T cells (Treg) play an important role in controlling and prevention of endometriosis through regulating immune responses. Treg cells are regulated by the forkhead box P3 () gene. The aim of this study is to monitor any changes in gene expression and epigenetic profile of ) in endometriosis. - Source: PubMed
Publication date: 2026/08/08
Chegeni SamanehFavaedi RahaIrian SaeedBajool NiloofarRamezanali FaribaKarimi GildaAmirchaghmaghi ElhamShahhoseini Maryam - Acute kidney injury (AKI) is sustained by reciprocal amplification of oxidative stress, innate immune signaling, and maladaptive immune-parenchymal crosstalk. Here, we developed a lipid nanoparticle containing a ceria nanozyme and a STING-targeting CasRx plasmid and functionalized it with D4F, an 18-residue apolipoprotein A-I mimetic peptide composed of D-amino acids. The resulting D4F-CeO@LNP-CasRx(STING) formulation retained radical-scavenging activity, supported CasRx encapsulation, and showed enhanced cellular and renal delivery. In macrophages, the formulation reduced oxidative stress and total STING abundance together with downstream TBK1 and IRF3 phosphorylation, shifted the CD86/CD206 profile toward a less inflammatory state, and altered the secretome in a manner that protected hypoxia-challenged tubular epithelial cells. In kidney organoids and peripheral-blood-mononuclear-cell-coupled organoid cultures, D4F functionalization improved intratissue accumulation, increased the frequency of CD4FOXP3 T cells, and attenuated the hypoxia-associated DNA damage response and tubular injury. In mice with renal ischemia-reperfusion injury, treatment reduced STING signaling in CD11b renal macrophages, improved renal function and histology, and lowered whole-kidney inflammatory and injury readouts. Spatial transcriptomic and proteomic analyses were consistent with contraction of inflammatory immune states and restoration of repair-associated programs. These findings support a DNA-delivering nanozyme strategy for renal immune-niche modulation in AKI. - Source: PubMed
Publication date: 2026/09/06
Chen WeiboLi MingWang XueshengSun JiajiaZhang ZiyuanGong YongfengShi BenkangYu NengwangMao YunuoZhao ShengtianZhang XiulinGuo Liqiang - Myo-inositol (MI) is involved in the regulation of key immune cell activities, including signaling pathways and cellular processes. Although immune cell distribution and cytokine expression are key determinants of immune competence in laying hens, the potential role of MI in regulating these parameters is largely unexplored. Thus, this study investigated the effects of dietary MI on the immune system of laying hens. At the age of 26 wk, corresponding to the peak laying period, 40 Lohmann Brown-Classic (LB) and 40 Lohmann LSL-Classic (LSL) hens received a maize-soybean meal-based diet either without (MI0) or with 1 (MI1), 2 (MI2) or 3 (MI3) g supplemented MI/kg feed for 4 wk, resulting in a 2 × 4 factorial design. We measured numbers of various leukocytes in blood, spleen and cecal tonsils, lymphocyte functionality and gene expression of pro- and anti-inflammatory cytokines. Dietary MI supplementation resulted in cell type-, strain- and concentration-specific effects, including increased circulating B cells in LSL hens fed with MI2, reduced splenic B cells in LB hens with MI1 and MI2 and lower CD4CD25 cells in the cecal tonsils of both strains with MI2. Strain-specific modulation of foxp3 and IL-12 gene expression was also observed. However, neither diet × strain interaction nor dietary MI revealed a clear dose-response relationship. On the contrary, immunological differences between the two strains, irrespective of MI supplementation, were highly prominent and are consistent with previous studies, with a generally higher innate immune response in LB hens, and a more specific and cellular immune response in LSL hens. Overall, our findings indicate that dietary MI supplementation does not broadly alter immune responses in laying hens but can modulate specific immune parameters in a strain-dependent manner. Despite the limited impact, dietary MI may still represent a potential approach to support more balanced immune responses. The results further emphasize immunological, physiological and metabolic variations between the two strains and the importance of genetic background when evaluating nutritional strategies for immune modulation. - Source: PubMed
Publication date: 2026/08/05
Wallauch NadineSchmucker SonjaHofmann TanjaSommerfeld VeraHasselmann MartinHuber KorinnaRodehutscord MarkusStefanski Volker - Mesenchymal stem cells (MSCs) exhibit potent immunomodulatory properties, yet their precise mechanisms in alleviating Echinococcus multilocularis-induced hepatic inflammation and fibrosis in Alveolar Echinococcosis (AE) remain elusive. This study aimed to elucidate the immunoregulatory mechanisms underlying MSCs therapy in AE. Using an AE mouse model, we demonstrated that MSCs administration significantly ameliorated liver histopathology, attenuated fibrosis, and restored liver function. Molecular analyses revealed that AE infection promoted a pro-inflammatory profile (elevated RORγt and IFN-γ) while suppressing regulatory factors (FOXP3, TGF-β1, IL-10, CNTN1, and Gilz), effects that were robustly reversed by MSCs treatment. In vitro, co-culture of CNTN1-knockdown MSCs with E. multilocularis antigen-stimulated CD4 T cells demonstrated that CNTN1 deficiency impaired MSCs-mediated immunoregulation, decreased IL-10 secretion, and disrupted the Th17/Treg balance. Mechanistically, dual-luciferase reporter assays confirmed that CNTN1 directly activates the Gilz promoter. Collectively, our findings identify the CNTN1/Gilz signaling axis as an essential mediator of MSCs immunomodulation, providing novel mechanistic insights into the therapeutic efficacy of MSCs against E. multilocularis-induced hepatic injury. - Source: PubMed
Publication date: 2026/09/04
Chong ShiguiGao WenhuaLei ShixinHe YulinZhao Yumin - Metal complexes possess unique spatial coordination frameworks and tunable biological functions, rendering them promising candidates for antitumor drug development. Herein, we rationally designed and synthesized a novel copper(II) complex Cu1 with the molecular formula Cu1(Cu(L)₂(ClO₄)₂·2H₂O, C₃₆H₂₆Br₂Cl₂CuN₈O₁₀S₂, where the ligand L corresponds to 2-([2,2':6',2″-terpyridin]-4'-yl)-4-bromothiazole. We systematically characterized its antitumor potency toward triple-negative breast cancer (TNBC) and dissected the underlying immunomodulatory mechanisms. UV-vis absorption titration and viscosity assays validated that Cu1 binds tightly to duplex DNA primarily via an intercalative binding mode. In cellular experiments, Cu1 exhibited potent cytotoxicity against both MDA-MB-231 and 4T1 cells, accompanied by pronounced nuclear accumulation and DNA damage. Mechanistically, Cu1 triggered massive intracellular reactive oxygen species (ROS) accumulation, activated the cGAS-STING axis coupled with endoplasmic reticulum (ER) stress, and elicited canonical immunogenic cell death (ICD), as validated by calreticulin (CRT) membrane translocation, HMGB1 cytoplasmic release, and elevated extracellular ATP secretion. Furthermore, Cu1 initiated Caspase-1/GSDMD-mediated pyroptosis. In both tumor vaccination and 4T1 orthotopic tumor-bearing mouse models, Cu1 displayed robust in vivo antitumor activity by orchestrating systemic antitumor immunity: it promoted dendritic cell (DC) maturation, boosted intratumoral CD8+ T cell infiltration, diminished immunosuppressive Foxp3+ regulatory T cells (Tregs), and established long-lasting tumor-specific immune memory. Collectively, Cu1 represents a multifunctional copper coordination complex that integrates direct tumoricidal activity and immunoregulatory capacity. This work delivers comprehensive experimental evidence supporting the translational development of copper-based therapeutic agents for TNBC chemoimmunotherapy. - Source: PubMed
Publication date: 2026/09/02
Wang BishuWang TaoLiu DongboYu ZhijieDu KejieWang JinquanFeng Tao