FOXP3 (229_250)
- Known as:
- FOXP3 (229_250)
- Catalog number:
- AP10074PU-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- FOXP3 (229_250)
Related genes to: FOXP3 (229_250)
- 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: FOXP3 (229_250)
(+)-cis,trans-Abscisic Acid (ABA)(+)-cis,trans-Abscisic Acid (ABA)(-)-Indolactam V0.9 Cu Ft （20L) 12x12x11" 250 °C Vacuum Drying Oven0.9 Cu Ft （20L) 12x12x11" 250 °C Vacuum Drying Oven1 Kb DNA Marker1-step Polymer HISTO-STAT; HRP anti Hamster (Secondary Reagent Component) for staining Hamster antibodies, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Chicken (Secondary Reagent Component) for staining Chicken antibodies, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Goat (Secondary Reagent Component) for staining Goat antibodies, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Mouse Adsorbed (Secondary Reagent Component) for staining Rat antibody- on- Mouse tissues, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Mouse Secondary Reagent Component) for staining Mouse and Rat antibodies, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Rat (SecondaryReagent Component) for staining Rat antibodies, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Rat Adsorbed (Secondary Reagent Component) for staining Mouse antibodies- on-Rat tissue, 250 slides plus1-step Polymer HISTO-STAT; HRP anti Sheep (Secondary Reagent Component) for staining Sheep antibodies, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Rabbit (Secondary Reagent Component) for staining Rabbit antibodies, 250 plus slides Related articles to: FOXP3 (229_250)
- The T cell population size is stringently controlled before, during, and after immune responses, as improper cell death regulation can result in autoimmunity and immunodeficiency. RIPK1 is an important regulator of peripheral T cell survival and homeostasis. However, whether different peripheral T cell subsets show a differential requirement for RIPK1 and which programmed cell death pathway they engage in vivo remains unclear. In this study, we demonstrate that conditional ablation of Ripk1 in conventional T cells (Ripk1) causes peripheral T cell lymphopenia, as witnessed by a profound loss of naive CD4, naive CD8, and FoxP3 regulatory T cells. Interestingly, peripheral naive CD8 T cells in Ripk1 mice appear to undergo a selective pressure to retain RIPK1 expression following activation. Mixed bone marrow chimeras revealed a competitive survival disadvantage for naive, effector, and memory T cells lacking RIPK1. Additionally, tamoxifen-induced deletion of RIPK1 in CD4-expressing cells in adult life confirmed the importance of RIPK1 in post-thymic survival of CD4 T cells. Ripk1 mice showed no change in peripheral T cell subsets, demonstrating that the T cell lymphopenia was due to the scaffold function of RIPK1 rather than to its kinase activity. Enhanced numbers of Ripk1 naive T cells expressed the proliferation marker Ki-67 despite the peripheral lymphopenia and single-cell RNA sequencing revealed T cell-specific transcriptomic alterations that were reverted by additional caspase-8 deficiency. Furthermore, Ripk1Casp8 and Ripk1Tnfr1 double-knockout mice rescued the peripheral T cell lymphopenia, revealing that RIPK1-deficient naive CD4 and CD8 cells and FoxP3 regulatory T cells specifically die from TNF- and caspase-8-mediated apoptosis in vivo. Altogether, our findings emphasize the essential role of RIPK1 as a scaffold in maintaining the peripheral T cell compartment and preventing TNFR1-induced apoptosis. - Source: PubMed
Publication date: 2024/05/11
Huysentruyt JelleSteels WolfRuiz Perez MarioVerstraeten BrunoVadi MikeDivert TatyanaFlies KayleighTakahashi NozomiLambrecht Bart NDeclercq WimVanden Berghe TomMaelfait JonathanVandenabeele PeterTougaard Peter - Myasthenia gravis (MG) is an immune-mediated disease frequently associated with thymic changes. Increased T helper 17 (Th17) cell activity and dysfunctional regulatory T (Treg) cells have been demonstrated in subgroups of MG. On the other hand, hypoxia-inducible factor 1 (HIF-1) has been shown to regulate the Th17/Treg balance by inducing Th17 differentiation while attenuating Treg development. To identify the underlying mechanisms of different thymic pathologies in MG development, we evaluated thymic samples from thymoma-associated myasthenia gravis (TAMG), MG with hyperplasia (TFH-MG) and thymoma without MG (TOMA) patients. Differential gene expression analysis revealed that TAMG and TFH-MG cells are associated with different functional pathways. A higher RORC/FOXP3 ratio provided evidence for Th17/Treg imbalance in TAMG potentially related to increased HIF1A. The hypoxic microenvironment in thymoma may be a driver of TAMG by increasing HIF1A. These findings may lead to new therapeutic approaches targeting HIF1A in the development of TAMG. - Source: PubMed
Publication date: 2024/05/11
Altınönder İlaydaKaya MustafaYentür Sibel PÇakar ArmanDurmuş HacerYegen GülçinÖzkan BerkerParman YeşimSawalha Amr HSaruhan-Direskeneli Guher - Cepharanthin alone or in combination with glucocorticoid (GC) has been used to treat chronic immune thrombocytopenia (ITP) since the 1990s. Cepharanthine (CEP) is one of the main active components of Cepharanthin. The purpose of this study was to investigate the effects of CEP on GC pharmacodynamics on immune cells and analyse the possible action mechanism of their interactions. - Source: PubMed
Publication date: 2024/05/11
Xu WenchengChen ShuheWang XiaoqinMin JinwenTanaka SachikoOnda KenjiSugiyama KentaroYamada HarukiHirano Toshihiko - Epstein-Barr virus (EBV) DNA is known to be shed upon reactivation of latent EBV. Based on our previous findings linking Toll-like receptor-9 (TLR9) to an EBV DNA-driven surge in IL-17A production, we aimed to examine the therapeutic potential of TLR9 inhibition in EBV DNA-exacerbated arthritis in a collagen-induced arthritis (CIA) mouse model. C57BL/6J mice were administered either collagen, EBV DNA + collagen, EBV DNA + collagen + TLR9 inhibitor, or only the TLR9 inhibitor. After 70 days, paw thicknesses, clinical scores, and gripping strength were recorded. Moreover, affected joints, footpads, and colons were histologically scored. Furthermore, the number of cells co-expressing IL-17A, IFN-γ, and FOXP3 in joint sections was determined by immunofluorescence assays. Significantly decreased paw thicknesses, clinical scores, and histological scores with a significantly increased gripping strength were observed in the group receiving EBV DNA + collagen + TLR9 inhibitor, compared to those receiving EBV DNA + collagen. Similarly, this group showed decreased IL-17A+ IFN-γ+, IL-17A+ FOXP3+, and IL-17A+ IFN-γ+ FOXP3+ foci counts in joints. We show that inhibiting TLR9 limits the exacerbation of arthritis induced by EBV DNA in a CIA mouse model, suggesting that TLR9 could be a potential therapeutic target for rheumatoid arthritis management in EBV-infected individuals. - Source: PubMed
Publication date: 2024/04/25
Sherri NourAssaf RayanBitar Elio RZnait SabahBorghol Abdul HamidKassem AyaRahal Elias A - TIICs are critical components of the TME and are used to estimate prognostic and treatment responses in many malignancies. TIICs in the tumor microenvironment are assessed and quantified by categorizing immune cells into three subtypes: CD66b+ tumor-associated neutrophils (TANs), FoxP3+ regulatory T cells (Tregs), and CD163+ tumor-associated macrophages (TAMs). In addition, many cancers have tumor-infiltrating M1 and M2 macrophages, neutrophils (Neu), CD4+ T cells (T-helper), CD8+ T cells (T-cytotoxic), eosinophils, and mast cells. A variety of clinical treatments have linked tumor immune cell infiltration (ICI) to immunotherapy receptivity and prognosis. To improve the therapeutic effectiveness of immune-modulating drugs in a wider cancer patient population, immune cells and their interactions in the TME must be better understood. This study examines the clinicopathological effects of TIICs in overcoming tumor-mediated immunosuppression to boost antitumor immune responses and improve cancer prognosis. We successfully analyzed the predictive and prognostic usefulness of TIICs alongside TMB and ICI scores to identify cancer's varied immune landscapes. Traditionally, immune cell infiltration was quantified using flow cytometry, immunohistochemistry, gene set enrichment analysis (GSEA), CIBERSORT, ESTIMATE, and other platforms that use integrated immune gene sets from previously published studies. We have also thoroughly examined traditional limitations and newly created unsupervised clustering and deconvolution techniques (SpatialVizScore and ProTICS). These methods predict patient outcomes and treatment responses better. These models may also identify individuals who may benefit more from adjuvant or neoadjuvant treatment. Overall, we think that the significant contribution of TIICs in cancer will greatly benefit postoperative follow-up, therapy, interventions, and informed choices on customized cancer medicines. - Source: PubMed
Publication date: 2024/04/23
Dakal Tikam ChandGeorge NancyXu CaimingSuravajhala PrashanthKumar Abhishek