Ask about this productRelated genes to: IL17D antibody
- 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: IL17D antibody
Related articles to: IL17D antibody
- 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
Wang XiaolingHuang YoucaiLuo TingtingLiu QinxianTian YuHu XiaoyuZheng YiFang ShuminTu YanyangZhen HainingGuo Yu - The spleen is the principal site of immune hematopoiesis and a major target of Streptococcus agalactiae (S. agalactiae) attack in Nile tilapia (Oreochromis niloticus). However, the immune-regulatory mechanisms employed by this organ against S. agalactiae remain unclear. In this study, integrated transcriptomic analysis of spleen tissue identified 27 genes-among them the core cytokines IL-6, CXCL3 and IL1R2-that responded to S. agalactiae challenge. Genome-wide mining subsequently revealed a total of 27 IL-family members in Nile tilapia. Synteny and chromosomal location analyses indicated that expansion of the family was associated with tandem and whole-genome duplication events. The expression levels of IL-1β, IL-8, CXCL3, and IL-34 were higher than those of other IL-family members in tilapia spleen. Following S. agalactiae infection, IL-6, IL-8, IL-8L, IL-12a, and IL-17D were significantly up-regulated, whereas CXCL3 was markedly down-regulated at 24 h post-infection (hpi). Functional enrichment analysis showed that the 27 genes that respond to S. agalactiae were over-represented in the IL-17 signaling pathway. Co-treatment of primary spleen cells with an IL-17A antagonist attenuated the S. agalactiae-induced up-regulation of IL-6, IL-8, and IL8-like. Bisulfite-sequencing PCR further revealed that putative CpG islands within the IL-17D promoter were demethylated in the spleen following S. agalactiae infection. Collectively, this study provides a theoretical framework for understanding IL-mediated immune regulation in the tilapia spleen during S. agalactiae infection. - Source: PubMed
Publication date: 2025/12/12
Wang ZhangHuang ShaoweiLiu HongTang ChenglinLiu ZhigangCao JianmengWang MiaoYi MengmengLu MaixinKe Xiaoli - Rabies, a zoonotic infectious disease causing central nervous system inflammation, remains a threat to public health in regions with limited medical resources. Vaccination effectively reduces rabies incidence and mortality, underscoring the need for vaccines that are cost-effective, immunogenic, protective, and safe. This study constructed a recombinant rabies virus (rRABV)-overexpressing glucocorticoid-induced tumor necrosis factor receptor ligand (GitrL), named rLBNSE-GitrL, using a reverse genetic operating system. rLBNSE-GitrL exhibited similar in vitro phenotypic characteristics and immune safety as the parent RABV (rLBNSE). This recombinant virus stimulated the production of a greater number of activated dendritic cells (DCs) compared to rLBNSE. The enhanced innate immune response induced by rLBNSE-GitrL may be mediated through the activation of innate immune-related signaling pathways, such as the tumor necrosis factor (TNF), and chemokine signaling pathways, and the upregulation of a series of innate immune-related genes, including MMP2, IL-6, CXCL9, TIMP1, IL-17d, and TNF-α. Consequently, rLBNSE-GitrL elicited significantly higher levels of RABV vaccine-induced virus-neutralizing antibodies (VNA), IgG, and IgM compared to rLBNSE as early as 3 days post-immunization (dpi), thereby improving the protective effect in mice. Collectively, the overexpression of GitrL facilitated the induction of early and potent antibody responses following RABV immunization. - Source: PubMed
Publication date: 2025/10/09
Wang YufangXing XiaoXiong ZhiminWang YongLiu YapingLi Yingying