Ask about this productRelated genes to: IL17B antibody
- Gene:
- IL17B NIH gene
- Name:
- interleukin 17B
- Previous symbol:
- -
- Synonyms:
- IL-17B, ZCYTO7, IL-20, MGC138900, MGC138901, NIRF
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-20
- Date modifiied:
- 2016-10-05
- Gene:
- IL17RB NIH gene
- Name:
- interleukin 17 receptor B
- Previous symbol:
- IL17BR
- Synonyms:
- IL17RH1, EVI27, CRL4
- Chromosome:
- 3p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-18
- Date modifiied:
- 2015-08-25
Related products to: IL17B antibody
Related articles to: IL17B antibody
- Immune checkpoint inhibitor (ICI)-based combinations have reshaped systemic therapy for unresectable hepatocellular carcinoma (HCC), yet durable responses remain limited, underscoring the need for mechanism-driven partners that reprogram the cirrhosis-conditioned tumor microenvironment. Here, we synthesize evidence supporting IL-17 family signaling as such a tractable axis and emphasize three translational takeaways. First, "IL-17 blockade" is not a single intervention: canonical IL-17A/F signaling through IL-17RA/RC differs from non-canonical nodes, including IL-17C signaling via IL-17RA/IL-17RE and the dual-ligand IL-17RB node (IL-25 versus IL-17B), which can yield context-dependent-and potentially opposing-effects. Second, HCC-focused models implicate an IL-17A-STAT3-PD-L1 immune-evasion circuit and show that IL-17A neutralization can enhance the activity of PD-1/PD-L1 blockade, positioning IL-17A/F inhibition primarily as an ICI-sensitizing strategy. Third, we argue that clinical translation should prioritize biomarker-guided, etiology-aware early-phase studies with on-treatment pharmacodynamic readouts, rather than unselected monotherapy, while explicitly accounting for infection and gut-barrier risks in cirrhosis. - Source: PubMed
Publication date: 2026/05/28
Pastwińska JoannaKarwaciak IwonaKaraś KajaSałkowska AnnaRatajewski Marcin - 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 - Exposure to immune stress or lipopolysaccharide (LPS) during critical developmental stages like puberty may lead to gut microbiome dysbiosis and epigenetic dysregulation in mammary glands, affecting gene expression and potentially elevating breast cancer susceptibility in adulthood. Although LPS's adverse impacts on intestinal and brain functions are well-documented, its effects on mammary glands remain underexplored. Using an immunocompetent BALB/c mouse model, we administered an acute LPS dose (1.5 mg/kg body weight) during puberty. The study evaluated the long-term consequences of LPS exposure alone and combined with AHCC (Lentinula edodes cultured extract, 2 g/kg body weight/day) on DNA methylation patterns, cytokine profiles, and microRNA expression in mammary glands at 9 weeks of age. Analyses included DNA methylation sequencing, multiplex immunoassays, quantitative PCR, and image processing. Pubertal LPS exposure produced persistent molecular dysregulation in mammary glands, including differential DNA methylation (> 5% change vs. control; FDR-adjusted p < 0.05), elevated inflammatory mediators, and altered microRNA expression. Differentially methylated regions were enriched in regulatory features, with decreased methylation at transcription start sites, promoters, and 5' UTRs of genes implicated in mammary development and oncogenic signaling (including Vav3, Pdgfa, Pdgfc, Jag2, Hras, Ksr1, Il2rb, Il17b, and Il17rb) in the LPS group, whereas the AHCC + LPS group exhibited a shift toward hypermethylation at these loci (approximately 5%-10% decrease). Inflammatory profiling showed increased IL-17A/F (∼2-fold vs. control; p < 0.05), while microRNA analyses indicated reduced let-7a/c (∼30% vs. control; p < 0.05). Notably, miR-130a and miR-34a increased ∼1.5-fold across all treatment groups relative to control. Pubertal LPS exposure induces enduring epigenetic and inflammatory changes in mammary glands that may heighten breast cancer risk. AHCC's mitigating role indicates potential for dietary interventions to counteract these effects. - Source: PubMed
Yasavoli-Sharahi HamedShahbazi RoghayehAlsadi NawalSahebi Nasim BondarCuenin CyrilleCahais VincentChung Felicia Fei-LeiHerceg ZdenkoMatar Chantal - CRISPR/Cas9-based genome editing is an inexpensive and efficient tool for genetic modification. Here, we present a methodological approach for establishing interleukin-17 receptor B (IL17RB) knockout cell lines using CRISPR/Cas9-mediated genomic deletion. The IL17RB gene encodes for a cytokine receptor that specifically binds to IL17B and IL17E and is overexpressed in various cancers. The method involves CRISPR design, CRISPR cloning, delivery of the CRISPR clone into cells, and verification of IL17RB gene deletion by deletion screening primer design, genomic DNA extraction, and polymerase chain reaction (PCR). A similar approach can be used for generating mammalian cell lines with gene knockout for other genes of interest. - Source: PubMed
Hu OliviaProvvido AlessandroZhu Yan - The present study aimed to investigate the regulatory functions and mechanisms of human β-defensin 1 (hBD-1) in head and neck squamous cell carcinoma (HNSCC) through comprehensive bioinformatics analyses and experimental validation. Comprehensive bioinformatics analyses of TCGA database samples were performed, including DEFB1 expression profiling, clinical correlation analysis, prognostic evaluation, and pathway enrichment studies. The results demonstrated that DEFB1/hBD-1 expression was significantly downregulated in tumor tissues and negatively correlated with key genes in the IL-17 signaling pathway, while being associated with reduced lymph node metastasis and improved overall survival. Immunohistochemical validation confirmed low hBD-1 protein expression in HNSCC tissues. Assessment of hBD-1 expression across multiple HNSCC cell lines revealed consistently downregulated hBD-1 mRNA and protein levels. Functional experiments using stable hBD-1-overexpressing cell models demonstrated that hBD-1 overexpression significantly inhibited cell metabolic activity, clone formation, invasion, and migration while effectively inducing apoptosis. Mechanistic studies revealed that hBD-1 suppressed the IL-17B/IL-17RB/TRAF6/NF-κB signaling pathway by downregulating IL-17B and IL-17RB expression, inhibiting TRAF6 ubiquitination, and decreasing NF-κB pathway protein phosphorylation levels. In vivo xenograft experiments validated that hBD-1 overexpression significantly reduced tumor growth, volume, cell proliferation, and increased apoptosis. These findings collectively demonstrate that DEFB1/hBD-1 functions as a tumor suppressor in HNSCC through suppression of the IL-17B/IL-17RB/TRAF6/NF-κB axis, positioning it as a potential prognostic biomarker and therapeutic target for HNSCC management. - Source: PubMed
Publication date: 2025/09/03
Hu ShaonanLi SiminChen WenhaoDai GuangqinHuang XiuhongTian TaoRao YaxinNing WanchenDeng XinMujagund PrabhakarKreher DeborahSchmalz GerhardHuang ShaohongLiu Chufeng