Human Interleukin 17D,IL-17D ELISA Kit
- Known as:
- Human Interleukin 17D,Interleukin-17D Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-2162
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human Interleukin 17D IL-17D ELISA Kit
Related genes to: Human Interleukin 17D,IL-17D ELISA Kit
- Gene:
- IL17D NIH gene
- Name:
- interleukin 17D
- Previous symbol:
- -
- Synonyms:
- IL-22, IL-27, IL-17D, IL27, FLJ30846
- Chromosome:
- 13q12.11
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-02
- Date modifiied:
- 2018-09-10
Related products to: Human Interleukin 17D,IL-17D ELISA Kit
Related articles to: Human Interleukin 17D,IL-17D ELISA Kit
- Circular RNAs (circRNAs) play important roles in cancer. However, their roles in pancreatic ductal adenocarcinoma (PDAC) progression and therapeutic resistance are underexplored. Here, we investigated the roles and diagnostic potential of circGANAB in PDAC. - Source: PubMed
Publication date: 2026/05/23
Wong Chi HinPeña-Paladines Jessica JazminLuo ZhiyuanMa Chi YauLee Yee LamLin Zhi-XiuXian Yan-FangHollingsworth Michael ATo Ka-FaiChen Yangchao - The interleukin-17 (IL-17) family of cytokines comprises structurally distinct ligands and receptors which mediate immune responses at mucosal surfaces. The growing understanding of its regulatory functions beyond immunity, together with extensive genetic variation in protein-coding genes, raises the possibility that IL-17 cytokines participate in an even wider network of biologic processes. Despite successes of experimental approaches to chart IL-17 functions, inherent signaling complexities and crosstalk with multiple physiologic pathways obscure a full appreciation of the biological potential of IL-17. Here, we integrated comparative genomics, evolutionary rate covariation (ERC), and signatures of natural selection to resolve phylogenetic relationships between IL-17 ligands and receptors and discovered evidence for hidden signaling interactions. ERC analysis revealed putative ligand-receptor interactions for IL-17D and IL-17RC and suggested uncharacterized potential signaling mediator for the receptor IL-17REL, such as IL-17B. Signals of covariation extended beyond the IL-17 family to other genes encoding neurodevelopmental effectors and growth factors, emphasizing recurrent co-evolutionary patterns that delineate the immune and neuromodulatory roles of IL-17. These connections are underlined by signatures of positive selection in the disordered N-terminal domain of IL-17E and its cognate receptor, IL-17RB, key modulators of both type 2 immune response and neuronal function, suggesting functional consequences of this understudied domain. Together, our findings suggest that IL-17 biology is repeatedly impacted by lineage-specific selective pressures that dictate both immune and non-immune functions. By anchoring the expanding IL-17 field in an evolutionary framework, we propose a model for understanding the diversification and functional expansion of this and other cytokine families. - Source: PubMed
Publication date: 2026/04/14
Cho Steve SChoi Gloria BHuh Jun RElde Nels C - Systemic inflammation has been identified as a key factor in neurodegeneration but the value of circulating inflammatory proteins in dementia risk prediction and their causal role has not been elucidated. - Source: PubMed
Publication date: 2026/01/19
Abdolkarimi DorsaLiu YueGilchrist LachlanCalhas SaraWaters SheenaMarshall Charles RProitsi Petroula - Despite significant advancements in targeted therapy and immunotherapy that have markedly improved the survival of patients with non-small cell lung cancer (NSCLC), challenges such as tumor heterogeneity and therapeutic resistance persist. Ferroptosis, a unique form of iron-dependent programmed cell death driven by lipid peroxidation, has emerged as a promising therapeutic target for cancer treatment. Interleukin-17D (IL-17D), a member of the IL-17 cytokine family, is involved in regulating immune cell responses within the tumor microenvironment. However, its role in ferroptosis remains unclear. In this study, we demonstrated that high IL-17D expression in lung cancer cell lines is significantly associated with ferroptosis resistance and predicts poor prognosis of patients with lung cancer. Mechanistically, IL17D overexpression promotes the expression of ferroptosis resistance-related genes by enhancing the accessibility of nuclear transcription factor Y (NFY) complex binding sites, and reduces intracellular lipid peroxidation levels. Notably, upon treatment with ferroptosis inducers, IL-17D significantly upregulates peroxisome proliferator-activated receptor gamma (PPARγ) expression, promotes cellular lipid droplet accumulation, and elevates ATP levels in lung cancer cells. Importantly, pharmacological inhibition of the PPARγ pathway reverses IL-17D-induced ferroptosis resistance. Collectively, these findings uncover a novel mechanism whereby IL-17D regulates ferroptosis through PPARγ-dependent lipid metabolic reprogramming, highlighting the IL-17D-PPARγ axis as a promising therapeutic target to overcome ferroptosis resistance in lung cancer. - Source: PubMed
Publication date: 2026/01/05
Du WeiFeng XiaofanLiu YaruLi XueyingOuyang YuqingZhang HaokeLiu ZiheLu XiaonaCai SiyuYu ChunyanLiu QianruiDeng Weimin - Liver metastasis (LM) poses a formidable barrier to effective immunotherapy, largely due to its uniquely immunosuppressive microenvironment and resistance to immune checkpoint blockade (ICB).Among emerging mechanisms, WNT11, a non-canonical WNT ligand, has been identified as a preclinical modulator of immune evasion in LM. Acting through a calcium-dependent CAMKII signaling pathway axis, WNT11 suppresses CD8 T-cell recruitment via downregulation of chemokines such as CXCL10 and CCL4 and promotes M2-like macrophage polarization through IL17D induction. This dual mechanism contributes to the formation of an immune-excluded, tolerogenic niche that undermines the efficacy of anti-PD-1 therapies. Targeting the WNT11/CAMKII axis restores immune infiltration and sensitizes LM to ICB in preclinical models, highlighting a promising therapeutic strategy. Although no direct WNT11-targeted therapies are currently available, multiple pharmacological strategies targeting its proximal and downstream effectors-such as FZD/ROR, CAMKII, PKC/JNK/NFAT, and associated crosstalk pathways like TGF-β, IDO1, and myeloid axes-are under active exploration. Additionally, circulating WNT11 levels may also serve as a predictive biomarker for patient stratification and treatment monitoring. Despite challenges related to pathway complexity and tumor heterogeneity, this mini review synthesizes recent advances in understanding the WNT11-driven tumor-immune axis and proposes a translational roadmap for combination strategies to overcome ICB resistance in liver metastasis. - Source: PubMed
Publication date: 2025/12/04
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