| 2000 |
IL-17B was cloned and expressed as a novel cytokine (~27% amino acid identity to IL-17A). It stimulates TNF-α and IL-1β release from the monocytic cell line THP-1, binds to THP-1 cells by FACS analysis, but does not bind the human IL-17R extracellular domain and does not induce IL-6 from fibroblasts, indicating it signals through a distinct cognate receptor. |
Recombinant protein expression, cytokine induction assay (THP-1 cells), FACS binding assay, IL-17R binding assay |
Proceedings of the National Academy of Sciences of the United States of America |
High |
10639155
|
| 2007 |
IL-17B induces TNF-α production from mouse peritoneal exudate cells in vitro. In vivo, adoptive transfer of IL-17B-transduced CD4+ T cells exacerbated collagen-induced arthritis, and bone marrow chimeric mice expressing IL-17B showed elevated serum TNF-α and higher arthritis scores. Neutralization of IL-17B suppressed arthritis progression and bone destruction. |
In vitro cytokine assay (peritoneal exudate cells), adoptive T cell transfer, bone marrow chimera model, anti-IL-17B neutralizing antibody treatment in CIA mouse model |
Journal of immunology (Baltimore, Md. : 1950) |
Medium |
17982105
|
| 2015 |
IL-17B–IL-17RB signaling in pancreatic cancer activates ERK1/2 pathway to induce CCL20, CXCL1, IL-8, and TFF1 chemokine expression, promoting cancer cell invasion, macrophage and endothelial cell recruitment, and cancer cell survival at distant organs. Anti-IL-17RB monoclonal antibody blocked tumor metastasis and promoted survival in a mouse xenograft model. |
Ex vivo cancer cell assays, ERK1/2 pathway inhibition, anti-IL-17RB antibody treatment, mouse xenograft model |
The Journal of experimental medicine |
High |
25732306
|
| 2017 |
IL-17B–IL-17RB signaling promotes resistance to paclitaxel in breast cancer cells via ERK1/2 pathway activation, leading to upregulation of anti-apoptotic BCL-2 family proteins. ERK pathway inhibitor PD98059 completely abolished IL-17B-induced chemoresistance. In vivo, anti-IL-17RB antibody restored tumor chemosensitivity to paclitaxel. |
Breast cancer cell line treatment with recombinant IL-17B, ERK1/2 pathway inhibition (PD98059), anti-IL-17RB neutralizing antibody, in vivo mouse tumor model |
Oncotarget |
High |
29371916
|
| 2017 |
IL-17B activates NF-κB, STAT3, and β-catenin pathways in mesenchymal stem cells and induces expression of stemness-related genes Nanog, Sox2, and Oct4, leading to enhanced tumor-promoting effects including increased gastric cancer cell proliferation and migration. |
Recombinant IL-17B treatment of mesenchymal stem cells, pathway activation assays, co-culture/conditioned medium proliferation and migration assays |
Oncotarget |
Medium |
28145881
|
| 2018 |
IL-17B–IL-17RB signaling in lung cancer cells induces ERK phosphorylation, resulting in GSK3β inactivation and β-catenin upregulation. IL-17RB also participates in IL-17B synthesis via the ERK pathway, creating a positive feedback loop that enhances invasion and migration. |
IL-17RB overexpression in lung cancer cell lines, ERK/GSK3β/β-catenin pathway analysis, in vitro invasion/migration assays, in vivo metastasis model |
Cancer letters |
Medium |
29496538
|
| 2019 |
IL-17B uses both IL-17RA and IL-17RB receptor subunits to elicit type 2 cytokine secretion from innate type 2 lymphocytes, NKT cells, and CD4+ CRTH2+ Th2 cells in the human immune system. IL-17B can also augment IL-33-driven type 2 responses. This receptor requirement (IL-17RA + IL-17RB) mirrors that of IL-25/IL-17E. |
Human lymphocyte stimulation assays with recombinant IL-17B, receptor subunit dependency experiments, cytokine secretion assays |
Journal of immunology (Baltimore, Md. : 1950) |
Medium |
30770417
|
| 2021 |
IL-17B/IL-17RB signaling promotes self-renewal and tumorigenesis of gastric cancer stem cells by inducing K63-linked ubiquitination of Beclin-1, mediated by TRAF6 binding to Beclin-1, thereby activating autophagy. ATG7 knockdown reversed IL-17B-induced self-renewal. IL-17B also induced IL-17RB expression in cancer cells. |
Recombinant IL-17B treatment of gastric cancer spheroid cells, Co-IP (TRAF6–Beclin-1 binding), ubiquitination assay, ATG7 knockdown, autophagy markers (LC3, autophagosome formation), IL-17RB silencing, in vivo tumor growth assay |
Oncogene |
High |
33649532
|
| 2021 |
Tumor-derived IL-17B carried by extracellular vesicles activates pancreatic stellate cells (PSCs) and induces IL-17RB expression in PSCs. Activated PSCs increase oxidative phosphorylation while reducing mitochondrial turnover, then activate tumor cells in a feedback loop that increases tumor cell oxidative phosphorylation and decreases glycolysis partially via IL-6, accelerating tumor growth. |
Extracellular vesicle isolation and characterization, IL-17RB overexpression in PSCs, metabolic assays (oxidative phosphorylation, glycolysis), co-injection xenograft mouse model |
Cancers |
Medium |
34771503
|
| 2016 |
IL-17B induces IL-8 gene and protein expression in human bronchial epithelial cells (but not lung fibroblasts) via activation of Akt, p38 MAPK, ERK, and NF-κB signaling pathways. |
Recombinant IL-17B treatment of bronchial epithelial cells and fibroblasts, signaling pathway inhibition assays, IL-8 gene/protein expression measurement |
Clinical immunology (Orlando, Fla.) |
Medium |
28039016
|
| 2024 |
Schwann-cell-secreted IL-17B acts in an autocrine manner by binding IL-17RB to promote macrophage recruitment after peripheral nerve injury. Global or Schwann-cell-specific IL-17B deletion reduced macrophage infiltration, myelin clearance, and axon regeneration. IL-17B signaling was found to be defective in injured central nerves. |
Mlkl-/- and Sarm1-/- mouse comparison, IL-17B global and Schwann-cell-specific knockout mice, nerve injury model, macrophage infiltration and myelin clearance assays, axon regeneration assessment |
Cell reports |
High |
38341853
|
| 2024 |
IL-17B inhibits B cell activation and differentiation (germinal center B cells and plasma cells) in systemic lupus erythematosus by downregulating FASN-mediated lipid metabolism, thereby inhibiting the Toll-like receptor and interferon pathways. IL-17B deficiency aggravated lupus in lupus-prone mice; recombinant IL-17B alleviated disease. |
IL-17B knockout lupus-prone mice, recombinant IL-17B treatment, FASN inhibition/knockdown, B cell activation and differentiation assays, TLR/IFN pathway analysis |
JCI insight |
Medium |
39115936
|
| 2022 |
IL-17B enhances vascular endothelial necroptosis during deep vein thrombosis by upregulating RIP3 and MLKL expression and their phosphorylation. IL-17B promoted IL-6 and TNF-α production downstream of RIP3/MLKL, and this effect was abolished by siRIP3 or siMLKL. Anti-IL-17B antibody reduced necroptosis markers and thrombus formation. |
DVT mouse model (IVC ligation), IL-17B knockout mice, anti-IL-17B antibody treatment, siRIP3/siMLKL knockdown in OGD cells, phosphorylation assays for RIP3/MLKL |
Journal of immunology research |
Medium |
36046722
|
| 2025 |
IL-17B inhibits hepatocellular carcinoma (HCC) cell proliferation and colony formation through an AKT-dependent but NF-κB-independent mechanism, acting via its receptor IL-17RB. This inhibitory effect was not observed in melanoma cells with low IL-17RB expression. |
Recombinant IL-17B treatment of HCC cell lines, AKT pathway inhibition, NF-κB inhibition, proliferation and colony formation assays, comparison with IL-17RB-low melanoma cells |
Archivum immunologiae et therapiae experimentalis |
Low |
40544497
|
| 2025 |
hBD-1 overexpression suppresses the IL-17B/IL-17RB/TRAF6/NF-κB signaling axis in HNSCC by downregulating IL-17B and IL-17RB expression, inhibiting TRAF6 ubiquitination, and decreasing NF-κB pathway phosphorylation, thereby inhibiting tumor cell invasion, migration, and promoting apoptosis. |
Stable hBD-1-overexpressing HNSCC cell lines, ubiquitination assay for TRAF6, NF-κB phosphorylation assay, in vivo xenograft model |
Journal of cranio-maxillo-facial surgery |
Low |
40908208
|
| 2002 |
IL-17B mRNA and protein are primarily expressed in neuronal cell bodies and axons of human and mouse spinal cord, dorsal root ganglia, and brain, as determined by in situ hybridization and immunohistochemistry. Expression begins at embryonic day 11 in mice and peaks at day 15. |
Northern blot, in situ hybridization, immunohistochemistry, radiation hybrid mapping |
Neuromuscular disorders : NMD |
Medium |
11738356
|
| 2012 |
Recombinant human IL-17B protein binds to its receptor on THP-1 cells with high affinity (FACS), stimulates THP-1 cells to secrete IL-1β and TNF-α in a dose-dependent manner in vitro, and induces neutrophil influx into the peritoneal cavity in vivo upon intraperitoneal injection. |
Eukaryotic expression (293T cells), FACS receptor binding, ELISA for cytokine secretion, in vivo peritoneal neutrophil recruitment assay |
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology |
Low |
22394632
|
| 2026 |
IL-17B deficiency increases M1-type macrophage infiltration in UPEC-infected kidneys and worsens kidney injury. Recombinant IL-17B treatment reduces macrophage infiltration by modulating chemokine expression (CCL2, CCL3, CCL7), indicating IL-17B regulates macrophage recruitment through chemokine regulation. |
IL-17B knockout mice, UPEC infection model, macrophage phenotyping, recombinant IL-17B treatment, chemokine expression analysis |
Microbiology spectrum |
Medium |
42065596
|