Anti-Mouse_Rat Foxp3 FITC 25 ug
- Known as:
- Antibody toMouse_Rat Foxp3 fluorecein 25 ug
- Catalog number:
- 11-5773-80
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse_Rat Foxp3 FITC 25
Related genes to: Anti-Mouse_Rat Foxp3 FITC 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 FITC 25 ug
Related articles to: Anti-Mouse_Rat Foxp3 FITC 25 ug
- Purpose Efficacy of checkpoint inhibitors (e.g., pembrolizumab) in head and neck squamous cell carcinoma (HNSCC) is limited by cancer-associated fibroblasts (CAFs). This randomized, double-blind, placebo-controlled, phase 2 trial (NCT05323656) evaluated the efficacy and safety of the reactive oxygen species inhibitor setanaxib with pembrolizumab in patients with CAF-rich HNSCC. Patients and Methods Participants (≥18 years) with recurrent or metastatic HNSCC with CAF tumor levels ≥5% received setanaxib (800 mg orally bid) or placebo for ≤105 weeks, plus intravenous pembrolizumab (200 mg q3w). The primary outcome was best percentage change from baseline in tumor size. Secondary outcomes included progression-free survival (PFS), overall survival (OS), and changes in tumor levels of CAFs, CD8+ tumor-infiltrating lymphocytes (TILs), and FOXP3+ T-regulatory cells at week 9. Results Fifty-five participants (setanaxib, n = 27; placebo, n = 28) were treated. Least squares (LS) mean (SE) best percentage changes in tumor size from baseline values were -7.9% (9.3%) (setanaxib) and -12.9% (9.0%) (placebo) (LS mean difference [80% CI]: 5.1 [-11.9, 22.0]; P = 0.7008). PFS hazard ratio (HR) (80% CI) was 0.58 (0.38, 0.89), favoring setanaxib (P = 0.1023 [threshold <0.2]). OS HR (80% CI) was 0.45 (0.24, 0.85), also favoring setanaxib (P = 0.1057). Transcriptomic analyses identified a significant increase in CD8+ TILs with setanaxib (P = 0.037) but not placebo. There were 33 serious adverse events (16 setanaxib, 17 placebo), leading to four deaths (all placebo). Conclusions These improvements in PFS, OS, and CD8+ TILs can guide further setanaxib research in patients with solid tumors. - Source: PubMed
Publication date: 2026/10/01
Fayette JérômeThomas Gareth JDaste AmauryRotarski MaciejCastelo BeatrizRullan AntonioLevine AaronPhilipson RichardJenkins Benjamin HHarrington Kevin J - Microbiome-based therapeutics to treat enteric bacterial infections requires stable engraftment of transplanted beneficial bacteria that target and eliminate the pathogen. The host factors that determine whether a microbiome transplant engrafts remain largely unresolved. Here we demonstrate that Interleukin-10 (IL-10) signaling deficiency leads to impaired fecal microbiota transplantation (FMT) engraftment and failure to resolve infection in mice. In the absence of IL-10-mediated immunoregulation provided by Foxp3 T cells, increased IFN-γ signaling in the intestine leads to elevated production of reactive oxygen/nitrogen species (ROS/RNS) by neutrophils and epithelial cells that supports the growth of inflammation-tolerant microbes, inhibits FMT engraftment, and impairs resolution of FMT treatment success can be restored by antibody-mediated blockade of IFN-γ signaling, neutrophil depletion or inhibition of ROS/RNS production. Lastly, we developed an -mRNA-LNP immunotherapy to boost IL-10 signaling in FMT Non-Responsive mice and demonstrate that -mRNA-LNP administration is sufficient to restore FMT engraftment and subsequent resolution of . Combined, these data support a mechanism by which IL-10 released by T cells limits IFN-γ mediated intestinal inflammation thereby promoting an intestinal microenvironment receptive to FMT engraftment and resolution of . These data demonstrate that the host's immune status can be therapeutically modulated to improve microbiome-based approaches to treat infection. - Source: PubMed
Publication date: 2026/09/23
Mridha SubhamAlam Md ZahidulDenny Joshua EHulit Ellie NMaslanka Jeffrey RMdluli Nontokozo VTran-Ha MinhMears Kevin SBrown Daivon DAlameh Mohamad-GabrielAbt Michael C - The gut-joint axis is a central paradigm in spondyloarthritis, yet the cellular mechanisms linking intestinal and joint immunity remain poorly understood. One potential link is TCRαβ CD4 intraepithelial lymphocytes in the colon (cIELs) that can traffic to extraintestinal tissues, including the joint. Within an inflamed joint, trafficked cIELs display both regulatory and inflammatory capacity. We sought to determine whether this functional identity is determined by an impaired epithelium or shaped by the joint environment. - Source: PubMed
Publication date: 2026/09/30
Danielson Sarah MEck ConnorLiu SucaiJonsson Anna HelenaKuhn Kristine A - Spontaneous preterm birth (sPTB) is a leading cause of neonatal morbidity and mortality worldwide. Excessive NLRP3 inflammasome activation coupled with impaired regulatory T cell (Treg)-mediated immune tolerance may be associated with sPTB; however, whether probiotic-derived metabolites can modulate this immunological imbalance under in vitro conditions remains unclear. - Source: PubMed
Publication date: 2026/09/28
Wang XuemeiZhuang LinHuang HeyingChen JinXu JiaoWang Xiaoyin - The relationship between the tumor microenvironment, comprising programmed cell death-1 ligand-1 (PD-L1), CD8-positive tumor-infiltrating lymphocytes (CD8TIL), and FOXP3TIL, in patients with epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer (NSCLC) and its clinicopathological features and the efficacy of EGFR-tyrosine kinase inhibitors remain poorly understood. - Source: PubMed
Publication date: 2026/09/06
Mizutani MegumiMatsumoto YoshiyaOhe ChisatoSugimoto AkiraNagamine HiroakiTani YokoOka TakakoKaneda HiroyasuYamada KazuhiroWatanabe TetsuyaAsai KazuhisaKimura TatsuoShiohara MasanoriKohashi KenichiKawaguchi Tomoya