Human forkhead box P3,Foxp3 ELISA Kit
- Known as:
- Human forkhead box P3,Foxp3 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-0693
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human forkhead box P3 Foxp3 ELISA Kit
Related genes to: Human forkhead box P3,Foxp3 ELISA Kit
- 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: Human forkhead box P3,Foxp3 ELISA Kit
Related articles to: Human forkhead box P3,Foxp3 ELISA Kit
- Rheumatoid arthritis (RA) is a chronic autoimmune disease that causes joint inflammation, disability, and reduced quality of life. Current mesenchymal stem cell (MSC) therapies face limitations due to cell variability and lack of standardization, highlighting the need for effective, cell-free alternatives that replicate MSCs' immunomodulatory functions. This study aimed to enhance MSC secretion of regulatory factors to modulate inflammation in an RA model. - Source: PubMed
Publication date: 2026/06/29
Mirdamadian Sayed AminAbtahi Froushani Seyyed Meysam M - Postbiotics offer improved safety and stability over live probiotics for modulating intestinal immunity, yet the receptor-mediated mechanisms underlying mucosal tolerance remain unclear. Nucleotide-binding oligomerization domain 2 (NOD2), a cytosolic sensor of bacterial cell wall components and a major genetic risk factor for inflammatory bowel disease (IBD), may link microbial signals to regulatory immune programs. Here, we show that heat-killed Lactobacillus sakei CVL-001 (HK CVL-001) promotes intestinal homeostasis through NOD2 signaling. HK CVL-001, but not its culture supernatant, significantly alleviated dextran sulfate sodium (DSS)-induced colitis, whereas this protection was completely lost in NOD2 mice. Treatment suppressed pro-inflammatory cytokines (IL-6, IL-1β), increased IL-10, and expanded Foxp3 regulatory T cells (Tregs) and CD103 tolerogenic antigen-presenting cell (APC) populations. In vitro, HK CVL-001 directly induced CD103 expression in BMDCs in a NOD2-dependent manner, enhancing their capacity to drive Treg differentiation. This effect was accompanied by upregulation of Irf8 and Irf4, along with expansion of both CD11b and CD11b CD103 APC populations. A functional role for NOD2 signaling within CD11c APCs was confirmed using CD11c-Cre × NOD2 mice and adoptive transfer experiments. These findings support a NOD2-dependent CD11c APC-Treg regulatory axis underlying postbiotic-induced mucosal tolerance. - Source: PubMed
Publication date: 2026/06/27
Kim Dong-YeonLee Tae-SungJung Do-HyeonKim Yeong-JunLee Yun-JiSeo In-SuKim Wan-GyuHong Jung JooPark Jong-Hwan - This study uses single-cell RNA sequencing (scRNA-seq) profiling to explore the heterogeneity of CD4 T cells at the maternal-fetal interface in URM and normal pregnancy groups, and to investigate the cell subsets associated with URM and the underlying pathophysiological mechanisms. Ultimately, it was determined that CD4T cells present at the maternal-fetal interface of URM patients exhibited a significant increase in acute inflammatory response, pro-inflammatory cytokines, and chemokines secreted by macrophages. Additionally, immune plasticity was observed in Treg cells, with a decrease in the expression of CD25, an increase in the constituent ratio of exTreg, and a decrease in the function of Treg to inhibit the inflammation of effector cells. Furthermore, the decrease in Treg receptor CCR4 was found to reduce the ability of Treg migration and local inflammation. The combined presence of PD1IL-10 and TIGITFOXP3 subtypes in Treg also increased, leading to the inhibition of the decline of CD8 effector cells function. Endothelial cells within the URM group demonstrate elevated levels of CX3CR1, which promote the recruitment of CX3CR1+ cells from the bloodstream and their subsequent migration to tissues. CX3CR1-expressing CD8 T and CD4 T cells undergo differentiation into effector cells equipped with cytotoxic granules, ultimately resulting in vascular and tissue damage. Regulatory T cells play a crucial role in suppressing local inflammation and preserving maternal-fetal immune tolerance. These findings offer a more comprehensive understanding of the dysregulation of the decidual immune microenvironment in URM, potentially informing advancements in the diagnosis and management of this condition. - Source: PubMed
Publication date: 2026/06/26
Huimei WuZhaoyang YuXinwei WangYuting WuJinghang JiangMujun LiXiaoqian Fu - Canine prostate carcinoma (cPCA) is an aggressive malignancy with limited prognostic markers. This study aimed to comprehensively characterize immune-cell infiltration, glycolysis, hypoxia and oncogenic markers in cPCA and assess their clinical relevance. Tumour tissues from 26 dogs with cPCA and hyperplastic prostate tissues from seven dogs were analysed using immunohistochemistry. Five immune cell markers (CD3, CD20, CD8, Foxp3 and CD204) were quantitatively assessed, and the amounts of immunolabelling of monocarboxylate transporter 4 (MCT4), glucose transporter 1 (GLUT1), human epidermal growth factor receptor 2 and Ki-67 were evaluated through established scoring methods. Associations between progression-free survival and overall survival were analysed using univariate Cox regression. All tumours were infiltrated by multiple immune-cell subsets, characterized by marked intertumoral heterogeneity. Immune-cell densities were generally higher in cPCA than in hyperplastic prostate tissue. Compared with hyperplastic prostate tissue, cPCA showed lower MCT4 and higher GLUT1 expression. No significant associations were observed between immune-cell density or marker expression and clinical outcomes. The findings suggest that cPCA has widespread immune-cell infiltration and distinct metabolic features; however, individual immunohistochemical markers alone were insufficient to predict clinical outcomes. - Source: PubMed
Publication date: 2026/06/26
Kato TaikiSakurai MasashiIchimata MasanaoKagawa YumikoToyoda HirotoKatayama RyuzoHarada KeiFukazawa EriMatsuyama FukikoKobayashi TetsuyaMizuno TakuyaIgase Masaya - Myocardial infarction (MI) disrupts immune homeostasis by impairing the recruitment and suppressive function of regulatory T cells (Tregs), which are hard to restore to date. In this study, a dual-functional platform based on core-shell microgels (Ab/HAPA C-S MGs) was developed to enhance Tregs homing and function within the post-infarct environment. The surface-modified C-C motif chemokine ligand 17 (CCL17) antibody neutralized excess CCL17, thereby enabling targeted Tregs recruitment. Propionic acid (PA) was released via hydrolytic cleavage of an encapsulated prodrug precursor (HAPA) within the core to promote Tregs immunosuppressive activity through fatty acid oxidation. The platform ensured localized retention and release of PA, addressing the pharmacokinetic limitations characteristic of short-chain fatty acid (SCFAs). The Ab/HAPA@C-S MGs enhanced Tregs recruitment by 4.2-fold through CCL17 neutralization, while enzymatically released PA boosted Tregs immunosuppression with 1.8-fold higher Foxp3 expression . In MI models, treatment with Ab/HAPA@C-S MGs promoted a 2.4-fold increase in Tregs infiltration while reducing Th17 cells in infarcted region, ultimately improving cardiac functions and attenuating myocardial fibrosis. These findings show potential of the SCFA-based C-S MGs system on regulating the immunomodulation and cardiac tissue repair. - Source: PubMed
Publication date: 2026/06/16
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