Monkey forkhead box P3,Foxp3 ELISA Kit
- Known as:
- Monkey forkhead box P3,Foxp3 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- MF004
- Product Quantity:
- 96T
- Category:
- -
- Supplier:
- Meretciel
- Gene target:
- Monkey forkhead box P3 Foxp3 ELISA Kit
Ask about this productRelated genes to: Monkey 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: Monkey forkhead box P3,Foxp3 ELISA Kit
Human ELC ELISA KIT 96 TEST
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Size#10 Rubber Bands, 1Lb Box Pale Crepe Gold#10 Rubber Bands, 1Lb Box Pale Crepe Gold#10 Rubber Bands, 1Lb Box Pale Crepe Gold#30 Rubber Bands, 1Lb Box Pale Crepe Gold#30 Rubber Bands, 1Lb Box Pale Crepe Gold#30 Rubber Bands, 1Lb Box Pale Crepe Gold#33 Rubber Bands, 1 Lb Box Pale Crepe Gold#33 Rubber Bands, 1 Lb Box Pale Crepe Gold Related articles to: Monkey forkhead box P3,Foxp3 ELISA Kit
- Intestinal inflammation disrupts epithelial integrity, fuels antibiotic resistance, and underlies disorders such as inflammatory bowel disease. Lactobacillus species, established inhabitants of traditional and contemporary fermented foods, are increasingly viewed as bioactive cultures that shape host immunity and support formulation of next-generation functional foods. This review integrates multidisciplinary evidence from in vitro studies, animal models, human observations, and multi omics datasets to clarify how dietary or probiotic Lactobacillus strains alleviate gut inflammation. Particular attention is given to strain specific effects on T-helper/T-regulatory cell balance, suppression of TLR4-MyD88, NF-κB, MAPK, and NLRP3 signaling cascades, and the influence of food matrices, microencapsulation, dosage, and processing parameters on bacterial viability and efficacy, which are the factors central to food industry application. Across models, Lactobacillus consistently down regulates pro-inflammatory Th1/Th17 responses, while expanding forkhead box protein 3 (Foxp3⁺) T reg, leading to reduced TNF-α, IL-1β, and IL-6 and elevated IL-10 and TGF-β. Short chain fatty acids (SCFAs) and indole metabolites derived from fermentation further dampen NF-κB activity and reinforce epithelial barrier function. Food matrix studies show that dairy and cereal formulations enhance probiotic survival, whereas acidic beverages often require micro encapsulation; a daily intake of ~ 10 CFU appears both effective and safe. Taken together, these insights position Lactobacillus as a scientifically robust, industry ready tool for developing anti-inflammatory foods, prioritizing future work for well-designed human feeding trials that couple multi-omics read outs and optimizing strain matrix combinations. - Source: PubMed
Publication date: 2026/07/08
Kulyar Md FNaqvi Syed Umair Ali ShahBernotiene EivaAkhtar Muhammad - Regulatory T cells (Tregs) are key mediators of immune tolerance and play a critical role in limiting excessive immune activation in conditions such as autoimmunity, transplantation, and graft-versus-host disease. Tregs are broadly classified into thymic-derived Tregs (tTregs) and peripherally induced Tregs (pTregs), which differ in lineage stability, epigenetic regulation, and functional plasticity. The suppressive function of tTregs is supported by stable expression of the transcription factor FOXP3, reinforced by demethylation of the Treg-specific demethylated region (TSDR). In contrast, pTregs are more susceptible to inflammatory cytokine signaling, which can destabilize FOXP3 expression and compromise suppressive function. Tregs employ multiple mechanisms of immune regulation, including CTLA-4-mediated inhibition of co-stimulatory signaling, cytokine modulation, metabolic interference, and, in certain contexts, granzyme-dependent cytotoxicity. Advances in cellular engineering have enabled the development of next-generation Treg therapies, including ex vivo expanded polyclonal Tregs, antigen-specific Tregs, and chimeric antigen receptor (CAR)-modified Tregs. Early-stage clinical and preclinical studies indicate that these approaches are feasible and exhibit favorable safety profiles in transplantation and immune-mediated diseases. This review summarizes current understanding of Treg biology, mechanisms governing lineage stability, and emerging strategies to enhance Treg specificity, persistence, and suppressive capacity, while highlighting remaining translational challenges. - Source: PubMed
Publication date: 2026/07/08
Azhar Mohammad AsimMir Tanveer AhmadKhan Mohammad AfzalAlzhrani AlaaSalma JahanKazmi ShadabAssiri Abdullah MBroering Dieter CYaqinuddin Ahmed - Although vitamin D (VitD) exhibits anti-tumor activity in colorectal cancer (CRC) preclinically, its effects in the human tumor microenvironment (TME) remain unclear. We conducted a randomized, placebo-controlled trial of preoperative high-dose VitD supplementation in stage I-III colon cancer patients to assess its impact on the TME. Forty-two patients received either VitD3 (50,000 IU/day for 7 days, then 10,000 IU/day) or placebo before surgery. Spatial immune-profiling and assessment of VitD receptor (VDR) and CYP27B1 expression were performed on paired tumor samples from 24 patients. VitD significantly increased plasma 25-hydroxyvitamin D levels (P<0.001), increased CD3+CD8+ memory T cells (P=0.03), reduced CD3+CD4+FoxP3+ regulatory T cells (P=0.02) and spatially re-organized the TME, leading to greater T cell and tumor cell proximity. Post-treatment VDR expression was heterogeneous and decreased overall (P=0.02). Spatial transcriptomic profiling of post-treatment resections reflected predominantly repressive VDR activity. These findings support an immunomodulatory role for VitD, warranting further mechanistic investigation. - Source: PubMed
Publication date: 2026/07/08
Dias Costa AndressaKim SuryunHong Sung ChulYuan ChenQi XinranZhang JinmingBleday RonaldGoldberg JoelIrani JenniferMelnitchouk NelyaSicinska Ewa TLowder Kristen EThalappillil Jennifer STakashima YasutoshiVäyrynen Sara APayne Elizabeth MMeyerhardt Jeffrey AYurgelun Matthew BAbrams Thomas AColeman Emma CFitzpatrick BridgetGanser ChristineMetayer Katherine ABrais Lauren KShivdasani Ramesh AWolpin Brian MHollis Bruce WNowak Jonathan ANg Kimmie - Atopic dermatitis (AD) is characterized by dysregulated immune responses and persistent inflammation. Regulatory B cells (Bregs) suppress inflammation, but the metabolic mechanisms constraining their function in AD remain unclear. - Source: PubMed
Publication date: 2026/07/07
Lee Seung TaekKim Ha EunKim So-YeonLee Jong YeongNam Kyung-HwaKim Sang-HyunPark Jun-YoungChoi Jin Kyeong - Regulatory T cells (Tregs) are critical guardians of immune homeostasis that must operate in diverse and often inflammatory conditions. However, the mechanisms that Tregs use to maintain their stability and function, especially in response to the stresses of distinct microenvironments, remain incompletely understood. Previous work identified the repressive chromatin modification histone 3 lysine 27 trimethylation (H3K27me3) as a rheostat for Treg function. Here, we find that loss of H3K27me3 in Tregs activates the tumor suppressor p53. Stabilization of p53 using the MDM2 inhibitor Nutlin-3 protected Tregs from losing their master transcription factor FOXP3 in vitro when cultured with the T helper 17 cytokines interleukin-6 and interleukin-1β, while p53 deficiency rendered Tregs more prone to FOXP3 loss. Treg-specific p53 deficiency resulted in the accumulation of cells that had lost Foxp3 expression ("ex-Tregs") and a reduction of suppressive markers on Tregs specifically in the colon. Additionally, these mice exhibited inflammation in the colon at homeostasis and increased severity of induced colitis. These results demonstrate a specific role for p53 in the maintenance of Treg stability in inflammatory T helper 17-polarizing environments and present a possible target for improving Treg-based immunotherapies for diseases defined by intestinal inflammation, such as inflammatory bowel disease. - Source: PubMed
Silveria StephaniePeeters Janneke G CVickery JennaVeronezi Giovana M BRamachandran SrinivasDuPage Michel