Foxp3 Fixation_Permeabilization Concentrate and Diluent Kit
- Known as:
- Foxp3 Fixation_Permeabilization Concentrate Diluent Kit
- Catalog number:
- 00-5521-00
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Foxp3 Fixation_Permeabilization Concentrate and Diluent Kit
Related genes to: Foxp3 Fixation_Permeabilization Concentrate and Diluent 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
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- Esophageal squamous cell carcinoma (ESCC) remains a highly lethal malignancy with limited durable responses to current therapies. Our previous work showed that all-trans retinoic acid (ATRA) upregulates the deubiquitinase OTUD6B and suppresses ESCC stemness. Here, we integrated in vivo pharmacological treatment, single-cell RNA sequencing, bulk RNA sequencing, immunofluorescence, flow cytometry, and OTUD6B disruption to define how ATRA remodels ESCC tumors. In a syngeneic mEC25 tumor model, ATRA inhibited tumor growth, and the ATRA-plus-anti-PD-1 group showed greater tumor inhibition than the ATRA-alone group. Single-cell profiling of ATRA- and vehicle-treated tumors identified epithelial, stromal, lymphoid, and myeloid compartments and revealed extensive immune remodeling after ATRA treatment. ATRA reduced FOXP3-associated regulatory T-cell features, attenuated M2-like macrophage polarization, and expanded a CD74-high neutrophil state. In epithelial tumor cells, ATRA-regulated genes were enriched in ubiquitination-related protein homeostasis, including protein ubiquitination, ubiquitin-dependent protein catabolism, and proteasome-mediated degradation. These findings prompted transcriptomic analysis of human ESCC cells treated with ATRA or subjected to OTUD6B silencing. ATRA treatment was negatively associated with hallmark epithelial-mesenchymal transition (EMT) enrichment, whereas OTUD6B knockdown was positively associated with EMT enrichment. Importantly, OTUD6B disruption attenuated ATRA-associated tumor suppression and abolished ATRA-induced reductions in CD25FOXP3 regulatory cells and F4/80CD206 macrophages, as well as the induction of CD74 neutrophils. These data support a possible contribution of OTUD6B to ATRA responsiveness and provide a rationale for further evaluation of ATRA-based immunotherapy combinations in ESCC. - Source: PubMed
Publication date: 2026/10/05
Yang TianshuoHuang YingLiu YaxinWang YuqingZhu XinyuShi HaoyuDai SuliZhao LianmeiLi Lei - Regulatory T (Treg) cells play a key role in immune tolerance and homeostasis. They prevent exaggerated immune responses, autoimmunity, and are crucial in graft-versus-host responses. On the other hand, their presence in many tumors is associated with a poor prognosis. In aged individuals, Treg populations are modified with a strong bias toward an effector phenotype and a reduced number of naïve Treg cells, but little is known about the functionality of human Treg cells in old age. The low frequency of Treg cells in human peripheral blood is the main limitation to studying them. Therefore, the development of induced Treg (iTreg) cells has become a valuable tool for in vitro research on peripheral Treg cells. Following a gold-standard protocol to generate iTreg in vitro, we aimed to investigate age-related differences in the generation of iTreg cells. However, we detected some unexpected results regarding Foxp3 induction and iTreg functionality. We found no differences in Foxp3 CD4 generated cells between young and older individuals. Surprisingly, the presence of the cytokine TGF-β did not play a role in either Foxp3 expression levels or in the suppressive activity of the resulting cells, regardless of the age of the donors. Therefore, we hypothesize that Foxp3 alone does not adequately define bona fide iTreg cells, and the presence of TGF-β is not essential for the in vitro differentiation of human conventional CD4 T cells into suppressive Foxp3 cells. - Source: PubMed
Publication date: 2026/10/05
Muller LynnBleher JanaWeinberger BirgitRocamora-Reverte Lourdes - Regulatory T cells (Tregs) control immune responses to autoantigens and play a key role in suppressing autoimmune reactions during the development of autoimmune diseases. One of the approaches to personalized regenerative therapy for autoimmune diseases is enhancing the proliferative and suppressive activities of Tregs . The transcription factor Forkhead box protein P3 (FoxP3) is a key regulator of the proliferative and suppressive activities of Tregs. FoxP3 pre-mRNA undergoes alternative splicing, and the full-length splice variant stimulates Treg proliferation and suppressive activity. In this study, we used cells obtained from three healthy donors and three patients with multiple sclerosis to compared the levels of FoxP3 splice variants in Tregs during their expansion (expanded Tregs, eTregs) and Tregs generated by transformation of CD4 T cells (transformed Tregs, tTregs). The full-length FoxP3 splice variant predominated in tTregs during the transformation process, which was accompanied by the increased proliferative and suppressive activities of these cells. In contrast, expansion of eTregs did not alter the proportions of FoxP3 splice variants; these cells proliferated less actively and exhibited lower suppressive activity than tTregs. Our findings demonstrate that transformation of CD4 T cells into Tregs is accompanied by an increase in the proportion of the full-length FoxP3 splice variant. Therefore, transformation may represent a more effective strategy than expansion of mature Tregs for generation of highly proliferative and suppressive cells in regenerative medicine. - Source: PubMed
Blinova Varvara GGladilina Yulia AShishparenok Anastasiya NEliseeva Daria DZhdanov Dmitry D - Cerebral ischemia-reperfusion (CIR) affects multiple organs, with lung injury being particularly prevalent. Formononetin, derived from legumes, has multiple pharmacological effects and demonstrated potential for the treatment of neurological diseases. However, its effects on CIR-induced lung injury are unknown. - Source: PubMed
Publication date: 2026/09/29
Chen LuyingZhou YajieYan DanLou LingyunZhou RenzhiChen HuijunWang Saibin - Pemphigoid diseases (PDs) are antibody-mediated autoimmune blistering diseases caused by loss of tolerance to basement membrane proteins such as type VII collagen (COL7), triggering pathogenic T and B cell responses. The contribution of regulatory T cells (T) to disease resistance remains unclear. Using a COL7 immunization-induced PD mouse model, we show that transient T depletion breaks tolerance and induces skin blistering in otherwise PD-resistant H2 mice. Disease occurred predominantly in females and was associated with impaired T recovery, early skin inflammation, altered B-cell homeostasis, and antigen-specific CD154 T cells. These findings identify T as critical regulators of susceptibility to PD. - Source: PubMed
Publication date: 2026/10/02
Pigors ManuelaGross NatalieOgunsulire Iretiolu MPatzelt SabrinaSzymczak SilkeLudwig Ralf JBieber KatjaScheffold AlexanderSchmidt Enno