Anti-Mouse CD127 FITC 100 ug
- Known as:
- Antibody toMouse CD127 fluorecein 100 ug
- Catalog number:
- 11-1271-82
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD127 FITC 100
Related genes to: Anti-Mouse CD127 FITC 100 ug
- Gene:
- IL7R NIH gene
- Name:
- interleukin 7 receptor
- Previous symbol:
- -
- Synonyms:
- CD127, IL7RA
- Chromosome:
- 5p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-07
- Date modifiied:
- 2019-04-23
Related products to: Anti-Mouse CD127 FITC 100 ug
Related articles to: Anti-Mouse CD127 FITC 100 ug
- Calcific aortic valve disease (CAVD) is an active, cell-mediated disorder lacking effective medical therapy. The contribution of programmed cell death (PCD) to disease progression remains insufficiently characterized. This study aimed to characterize PCD-related transcriptomic features during CAVD progression and identify candidate molecular indicators associated with disease severity. - Source: PubMed
Publication date: 2026/06/23
Yu XianguanZhao YunyueChen ZefengTang LeileXiong Zhaojun - Dermal group 2 innate lymphoid cells (dILC2s) contribute to skin homeostasis and inflammatory responses, yet they are frequently studied in Rag1-deficient mice in which the dILC2 compartment may itself be altered. - Source: PubMed
Publication date: 2026/07/20
Saleh Mohamed MLiao KexinBraun AndreaSalinas GabrielaSchön Michael PDasari PrasadBuhl Timo - Regulatory CD4+ T cells (Tregs), as defined by expression of the transcription factor Foxp3, strongly depend on the cytokine interleukin 2 (IL-2) for their survival and function and are often identified by the combination of high IL-2Rα (CD25) and low IL-7Rα (CD127) expression. Nevertheless, subsets expressing higher levels of IL-7Rα have been described, and IL-7 signaling does play a role in Treg function in some specific biologic contexts and tissues. The precise role of IL-7Rα-expressing Tregs in autoimmunity remains poorly defined though, potentially hampering current efforts to develop IL-7Rα blockade for the treatment of various autoimmune diseases. To ask whether cell-intrinsic IL-7Rα expression in Tregs was required for their function during type 1 diabetes (T1D) development, we generated non-obese diabetic (NOD) mice in which IL-7Rα is exclusively deleted in Foxp3-expressing Tregs. In young NOD mice, IL-7Rα deficiency did not alter Treg numbers and phenotype. However, 100% of NOD mice with IL-7Rα-deficient Tregs became diabetic, while the T1D incidence is typically around 50-60% in our colony. This increased susceptibility for T1D indicates that IL-7Rα expression in Tregs is required to protect a subset of NOD mice against islet autoimmunity. At the time of T1D onset, CD4+ and CD8+ T cells from NOD mice with IL-7Rα-deficient Tregs showed increased IFN-γ and IL-2 cytokine production. Our data demonstrate that cell-intrinsic IL-7R signaling in Foxp3+ Tregs is required to suppress effector T cell responses and to prevent full penetrance of T1D in NOD mice. - Source: PubMed
Jones Iv Albert RSmith Peyton SDooms Hans - Shellfish allergy is the most common food allergy in adults and the third most common in children. γδ T cells have been identified as playing a critical role in antigen tolerance in allergic diseases in mouse models. In humans, γδ T cells may play a regulatory role in peanut immunotherapy, and their role in shrimp allergy remains unclear. We hypothesized γδ T cells play a regulatory role in shrimp allergic disease. We performed single cell RNA sequencing (scRNAseq) on peripheral cells from shrimp allergic (SA) and healthy control (HC) subjects after stimulation with shrimp tropomyosin. This revealed a significant expansion of γδ T cells with three distinct clusters. One γδ T cell cluster predominated in SA, characterized as CD8+ with a cytotoxic expression profile. We found significant upregulation of TGF-β1 and downregulation of IL-7R in SA-stimulated γδ T cells, and IL-10RA expression in stimulated SA total PBMCs. γδ T cells may play a role in shrimp allergic disease through lymphocyte-mediated cytotoxin signaling and cytokine-mediated signaling pathways, including TGFβ-1, IL7/TSLP-IL7R, and IL10-IL10R pathways. - Source: PubMed
Su Brenda BinJackson TylerBlackmon WarrenAmes HaroldHolt ChristopherAnagnostou AikateriniSzafron VibhaAnvari SaraLi HongjieDavis Carla M - The development and functional maintenance of CD8 T cells are metabolically regulated processes in which mitochondria serve as the central hub. Here, we identify glucose-regulated protein 75 (GRP75) as a critical mitochondrial regulator controlling these processes. Using T cell-specific Hspa9 (encodes GRP75) knockout mice, we demonstrate that GRP75 deficiency disrupts CD8 T cell fate, leading to defective T cell homeostasis and impaired memory differentiation. Mechanistically, impaired mitochondrial function in GRP75-deficient CD8 T cells leads to perturbation of IL-7R signaling and aberrant expression of effector-associated molecules. Further studies reveal that GRP75 deficiency leads to upregulation of interferon regulatory factor 4 (IRF4), a critical transcription factor for effector versus memory fate, which in turn suppresses memory CD8 T cell differentiation. Our findings establish GRP75 as a pivotal mitochondrial checkpoint that coordinates metabolic state and functional fate in CD8 T cells. - Source: PubMed
Publication date: 2026/07/31
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