Monkey IL-17F ELISA kit
- Known as:
- Monkey Interleukin-17F Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- CT503A
- Product Quantity:
- 5-plate*
- Category:
- -
- Supplier:
- U-CyTech
- Gene target:
- Monkey IL-17F ELISA kit
Related genes to: Monkey IL-17F ELISA kit
- Gene:
- IL17F NIH gene
- Name:
- interleukin 17F
- Previous symbol:
- -
- Synonyms:
- IL-17F, ML-1, ML1
- Chromosome:
- 6p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-03-18
- Date modifiied:
- 2019-04-23
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- It has previously been demonstrated that the nuclear factor of activated T cells (NFAT) is crucial for the development of tumors. Given OSCC's drug resistance and poor outcomes, identifying NFAT-associated prognostic genes is urgent for better treatment. - Source: PubMed
Tuerxun JulaitiAiniwaer AilimaierdanDing Tairan - While occult hepatitis B virus infection is a known risk factor for progressive liver diseases, the mechanistic basis for this association is poorly understood. To investigate this, we conducted a comparative study involving 40 OBI blood donors and 100 healthy blood donors to assess clinical parameters of liver fibrosis, including serum biomarkers, the FIB-4 index, and liver stiffness measurement. Transcriptome sequencing of peripheral blood mononuclear cells from these donors identified IL-17F as significantly upregulated in the OBI group. Mechanistically, we found that IL-17F was chiefly secreted by CD4 T cells upon HBcAg stimulation and functionally promoted the expression of key fibrosis-related cytokines and markers. Collectively, our study unveils a novel pathway wherein HBcAg induces CD4 T cells to secrete IL-17F, which in turn accelerates liver fibrogenesis, providing a mechanistic basis for OBI-associated liver disease.IMPORTANCEThis study reveals, for the first time, a novel mechanism by which OBI drives liver fibrosis, demonstrating that HBcAg stimulates CD4 T cells to secrete IL-17F, which in turn activates macrophages and hepatic stellate cells, thereby promoting liver inflammation and fibrosis. This discovery not only elucidates a key molecular pathway underlying OBI-related liver disease progression, but also provides an important theoretical foundation for developing IL-17F-targeted diagnostic approaches and anti-fibrotic therapies. - Source: PubMed
Publication date: 2026/07/17
Liu BochaoHuang JietingYang HualongLiao QiaoWang MinXu RuShan ZhengangZhong HuishanLiao FengfangLi TingtingLi ChengyaoLiang HuaqinFu YongshuiRong Xia - Psoriasis is a prototypical chronic inflammatory skin disease that illustrates fundamental interactions between innate and adaptive immune pathways. Central to its pathophysiology is the interleukin-23/interleukin-17 (IL-23/IL-17) axis, which is driven by both adaptive T helper 17 (Th17) cells and group 3 innate lymphoid cells (ILC3s). These cell populations share the ability to produce IL-17A, IL-17F, and IL-22, cytokines that activate keratinocytes, promote epidermal hyperproliferation, and sustain the inflammatory microenvironment characteristic of psoriatic lesions. While Th17 cells arise from antigen-driven adaptive immune responses and contribute to the persistence of chronic inflammation, ILC3s respond rapidly to cytokine signals such as IL-23 and provide an early, antigen-independent source of IL-17 and IL-22. The functional overlap and extensive crosstalk between these two cell types create a robust and self-amplifying inflammatory circuit. Increasing evidence suggests that psoriasis comprises immunological endotypes in which either Th17 cells or ILC3s may predominate, potentially contributing to clinical heterogeneity and differential responses to targeted therapies. Because psoriasis exemplifies the cooperation between innate and adaptive IL-17-producing lymphocytes, it provides a valuable model for understanding immune regulation in chronic inflammatory and autoimmune diseases. Elucidating the balance, redundancy, and plasticity between Th17 cells and ILC3s may therefore help refine disease stratification and guide future precision-based therapeutic strategies. - Source: PubMed
Publication date: 2026/07/02
Schön Michael P - Autoimmune uveitis is a vision-threatening inflammatory disorder driven by dysregulated T helper 17 (Th17) responses, yet therapeutic strategies targeting Th17 differentiation are lacking. Through transcriptomic screening of an experimental autoimmune uveitis (EAU) model and validation in peripheral blood mononuclear cells from Vogt-Koyanagi-Harada patients, we identified MAP1S (microtubule-associated protein 1S) as a pivotal, conserved regulator. Here, we demonstrate that MAP1S constrains pathogenic Th17 responses and alleviates EAU through a dual mechanism coordinating transcriptional control and autophagic degradation. Mechanistically, MAP1S binds to EGR2 (early growth response 2) and restrains its acetylation at Lys368, thereby suppressing (lipocalin 2) transcription. Besides, MAP1S facilitates autophagosome biogenesis and lysosomal trafficking, promoting the autophagic clearance of LCN2 protein. Notably, MAP1S deficiency enhances EGR2 acetylation, increases transcription, disrupts autophagosome trafficking, impairs LCN2 degradation, and promotes LCN2 accumulation, collectively driving Th17 polarization and exacerbating EAU pathology. Adoptive transfer of cervical lymph node cells from knockout mice reproduced severe disease in wild-type recipients. Moreover, pharmacological activation of MAP1S with spermidine suppressed Th17 responses and alleviated disease severity. Our findings establish MAP1S as a critical node integrating acetylation signaling of EGR2 and autophagic flux to govern LCN2 homeostasis and Th17 pathogenicity, revealing a promising therapeutic target for autoimmune uveitis and potentially other Th17-mediated diseases.: AAV: adeno-associated virus; ACOD1: aconitate decarboxylase 1; AU: autoimmune uveitis; BCL2: B cell leukemia/lymphoma 2; CDLNs: cervical draining lymph nodes; CFA: complete Freund's adjuvant; ChIP: chromatin immunoprecipitation; Co-IP: co-immunoprecipitation; CQ: chloroquine; EAU: experimental autoimmune uveitis; EGR2: early growth response 2; GDF15: growth differentiation factor 15; HDAC4: histone deacetylase 4; HDAC6: histone deacetylase 6; IL17: interleukin 17; IL17f: interleukin 17f; IL22: interleukin 22; K: lysine; KAT2A/GCN5: K(lysine) acetyltransferase 2A; KO: knockout; LCN2: lipocalin 2; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MAP1S: microtubule-associated protein 1S; MS: mass spectrometry; PBMC: peripheral blood mononuclear cell; PCR: polymerase chain rection; PPI: protein-protein interaction; PTX: pertussis toxin; qPCR: quantitative PCR; RT-qPCR: reverse transcription and quantitative real-time RCR; SAA3: serum amyloid A3; SPD: spermidine; Th1 cells: T helper 1 cells; Th17 cells: T helper 17 cells; TF: transcriptional factor; Tcells: regulatory T cells; VKH disease: Vogt-Koyanagi-Harada disease; WT: wild-type. - Source: PubMed
Publication date: 2026/07/23
Cai YingjunXie LihuiLi BowenChen BolinZou JingXu Huizhuo - Beta-thalassemia (β-Thal) is an inherited hemoglobin disorder caused by defective β-globin synthesis, resulting in ineffective erythropoiesis, chronic hemolytic anemia, and altered iron metabolism; it is highly prevalent in Iraq, a country with a complex and not fully characterized immunological profile. Inflammatory cytokine dysregulation in transfusion-dependent patients further compromises hematopoiesis, drives progressive iron overload, and perpetuates immune activation. This study aims to compare the gene expression and protein levels of seven cytokines - IL-1β, IL-4, IL-5, IL-12, IL-13, IL-17F, and TNF-α - between patients with beta-thalassemia and healthy controls. - Source: PubMed
Publication date: 2026/07/11
Mutlag Suzan SabbarAl-Tameemi Ghaith AOthman Mohammed Abdul-Mounther