Ask about this productRelated genes to: IL1b protein
- Gene:
- IL1B NIH gene
- Name:
- interleukin 1 beta
- Previous symbol:
- -
- Synonyms:
- IL1F2, IL-1B, IL1-BETA
- Chromosome:
- 2q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-03-31
- Date modifiied:
- 2016-10-05
Related products to: IL1b protein
Related articles to: IL1b protein
- Although radiation therapy (RT) remains one of the most effective treatments for patients with the lethal brain tumor glioblastoma (GBM), quite a number of patients show resistance or relapse shortly after RT. There is an urgent need to uncover the temporal and spatial dynamics of RT resistance during tumor progression and treatment. - Source: PubMed
Publication date: 2026/09/15
Wu LingxiangCheng LeiHuang BinHuang RunhengEzhilarasan RavesankerZhang JunxiaWu WeiWu GuojingYu BenqingGoodman Lindsey DJambhale AnanyaHu BaoliChen ApengZhu MengyanWu MinXia PengLiu QuanzhongYu MiaoZhao ZhengCheng ZhangchunWang NingLin FanZhou FengqiZhang Ze-YanDing YingwenChen JianQian XuWang XiuxingShi YuGumin JoyBhat KrishnaYung W K AlfredAldape Kenneth DVerhaak Roel G WLang Frederick FYou YongpingYang JiankaiWang QianghuSulman Erik P - Lung cancer is the second most prevalent malignancy in both sexes and remains the leading cause of cancer-related mortality. This study aimed to evaluate the expression profile of selected Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling-related genes and long non-coding RNAs (lncRNAs), particularly those involved in pro-inflammatory and autophagic pathways, in lung cancer tissues. - Source: PubMed
Publication date: 2026/09/08
Sayad ArezouMousazadeh MahsaHahem Nejad Mohammad AminMomeni Seyed SohaEslami SolatGhafouri-Fard Soudeh - L-proline (Pro) is a conditionally essential amino acid that has been reported to exert protective effects on intestinal health. This research investigated whether Pro supplementation reduces intestinal inflammation in weaned rabbits, and whether this effect involves the maintenance of the intestinal mucosal barrier and the composition of gut microbiota. A total of thirty weaned New Zealand White rabbits were randomly divided into five groups: a control group, an LPS-challenged model group, and three LPS-challenged groups receiving 0.5%, 1% or 2% Pro in their drinking water. Following the overall results of the study, 1% Pro was chosen for further investigation. Notably, 1% Pro supplementation significantly decreased the spleen index, alleviated colonic histopathological injury, enhanced the expression of the tight junction proteins Occludin and Zonula Occludens-1 (ZO-1), restored the population of goblet cells, decreased the colonic mRNA levels of the pro-inflammatory cytokines and , and increased the expression of the anti-inflammatory cytokine . Microbiome analysis revealed that Pro supplementation was associated with alterations in the dysbiotic gut ecosystem, including increased relative abundances of potentially beneficial genera such as , and , and decreased the relative abundance of opportunistic pathogens like . Overall, these results suggest that Pro functions as a microbiota-modulating immunonutrient that mitigates intestinal inflammation and supports the integrity of the mucosal barrier, likely through changes in gut microbial composition. - Source: PubMed
Publication date: 2026/09/01
He BiyanTao SimingXiang YilingXu CaixueYin YongtianHe XiaoxianMa XiaokangWu ZhenlongQin YingheLiu Ning - Immune dysregulation characterized by persistent myeloid activation and associated impairment of regulatory T cell (Treg) function contributes to inflammatory signaling across peripheral and central compartments in neurodegenerative diseases. We evaluated whether combining a glucagon-like peptide-1 receptor agonist (GLP-1RA; semaglutide) with low-dose interleukin-2 (LD-IL2) could modulate myeloid-associated transcript expression and enhance Treg-associated regulatory transcripts in a subacute lipopolysaccharide (LPS)-induced model of systemic and CNS inflammation. Mice received LPS once daily for 5 days, while GLP-1RA, LD-IL2, or combination treatment was initiated 24 h after LPS onset and continued daily. Splenic immune populations were quantified, and transcript expressions were assessed in magnetically enriched CD11b myeloid cells and CD4CD25 Tregs, as well as in cortex and hippocampus. As monotherapies, GLP-1RA reduced myeloid expansion with modest modulation of pro-inflammatory and anti-inflammatory myeloid transcripts, whereas LD-IL2 selectively enhanced Treg numbers and increased transcripts associated with Treg stability and suppressive regulation, including (CD25), , , (HELIOS), (CD39), and (CD73). Combination treatment significantly reduced LPS-induced myeloid , , and expression and increased expression. Combination treatment further enhanced Treg-associated (CD25), , and expression relative to monotherapies. In cortical and hippocampal tissues, combination treatment produced more robust modulation of inflammatory transcripts compared with effects observed with monotherapies, including reductions in and and increases in and (CD206) expression. Together, these findings demonstrate coordinated and complementary changes in peripheral immune-cell populations and myeloid inflammatory and Treg-associated regulatory transcripts and warrant further evaluation of this combination in inflammation-driven neurodegenerative disease. - Source: PubMed
Publication date: 2026/09/02
Thome Aaron DWang JinghongFaridar AlirezaZhao WeihuaSaetzler ValerieBeers David RAppel Stanley H - The progression of tuberculosis (TB) from a latent infection to an active disease involves intricate modifications in host immune, inflammatory, oxidative, and metabolic pathways. Ferroptosis represents a distinct form of regulated cell death that requires iron and is associated with excessive lipid peroxidation and has been associated with tissue damage in TB; however, its connection with host transcriptional changes during active TB is not fully understood. This study sought to identify and externally validate immune-inflammatory hub genes among differentially expressed genes (DEGs) in active TB that overlap with a ferroptosis-associated gene set derived from FerrDb, employing an integrated transcriptomic and systems-biology methodology. Differential expression analysis of GSE37250 revealed 1015 DEGs in active TB compared to latent TB, comprising 585 upregulated and 430 downregulated genes, and 93 DEGs in active TB compared to healthy controls, including 65 upregulated and 28 downregulated genes. Intersection analysis identified 94 DEGs common to the active TB versus latent TB comparison and the ferroptosis-associated gene set, and eight DEGs common to the active tuberculosis versus healthy-control comparison and the same gene set, with no genes shared across all three sets. Functional enrichment of the 94 intersection genes underscored immune response, defense response, stress response, Toll-like receptor signaling, NOD-like receptor signaling, IL-17 signaling, TNF signaling, glutathione metabolism, neutrophil degranulation, cytokine signaling, and antimicrobial metal sequestration. Protein-protein interaction analysis followed by cytoHubba prioritization identified 10 hub genes: IL1B, TLR4, CXCL10, MMP9, CYBB, MPO, CD36, LCN2, S100A8, and LTF. Subsequent to outcome-independent probe selection, external validation in GSE28623 demonstrated significant positive differential expression of LCN2, S100A8, and LTF, while GSE62525 showed significant positive differential expression of IL1B, TLR4, MMP9, MPO, LCN2, and LTF. LCN2 and LTF were significantly upregulated in both validation datasets, indicating the strongest cross-dataset reproducibility. These results identify an immune-inflammatory transcriptional network intersecting with ferroptosis-associated genes in active TB. Notably, the transcriptomic findings do not confirm ferroptotic cell death but suggest candidate genes and biological processes for future experimental exploration. - Source: PubMed
Publication date: 2026/08/29
Elsayim RashaAlqahtani Monerah S MAlaaullah Malek Hassan IbrahimBin Suaydan Reem AAbudouleh Esra'aMohamed Sami Habiballa AbdallaAlmuraikhi Nihal