Interleukin 1 beta

Overview

Interleukin-1 beta (IL-1β), encoded by the IL1B gene (Wikidata: Q411529), is a pleiotropic pro-inflammatory cytokine belonging to the interleukin-1 family of signaling proteins. It is produced predominantly by activated macrophages, monocytes, and dendritic cells, and plays a central role in orchestrating innate immune responses, fever, and systemic inflammation. IL-1β is synthesized as an inactive 31 kDa precursor (pro-IL-1β) that requires proteolytic cleavage by caspase-1 (CASP1) — a component of the NLRP3 inflammasome — to generate the biologically active 17 kDa mature form. Once secreted, IL-1β signals through its cognate receptor IL-1R1, activating downstream cascades including nuclear factor kappa B (NF-κB) and MAPK pathways to drive the transcription of genes encoding additional inflammatory mediators such as interleukin-6, tumor necrosis factor alpha, and prostaglandins.

Beyond its canonical role in acute immunity, IL-1β is a critical mediator of chronic inflammatory and fibrotic disease processes. Its sustained overproduction has been linked to the pathogenesis of rheumatoid arthritis, sepsis-associated organ injury, neurodegeneration, metabolic disease, and diabetic complications. The protein functions within complex cytokine networks alongside Tumour necrosis factor alpha, interleukin-6, and IL-18, and its activity is tightly regulated by endogenous antagonists such as IL-1Ra. Because of its broad pathological relevance, IL-1β has emerged as a high-priority therapeutic target, and its measurement — in serum, urine, or tissue homogenates — serves as a widely used pharmacodynamic and diagnostic biomarker across virtually every domain of biomedical research.

Focus of Latest Publications

Recent publications have examined interleukin-1 beta (IL-1β) as a marker and mediator of inflammatory pathology across several disease contexts. In neurodegeneration models, IL-1β was assessed alongside oxidative stress and the NLRP3 inflammasome in aluminum-induced memory impairment, where trans-anethole reduced IL-1β expression together with NLRP3 and TNF-α and was associated with improved cognitive performance and histopathological protection. A separate study of polystyrene nanoplastic exposure in mice linked hippocampal oxidative stress, microglial activation, and microglial extracellular trap formation to increased IL-1β and TNF-α, with N-acetylcysteine attenuating these changes and preventing neuronal ferroptosis and cognitive deficits.

IL-1β has also been investigated in renal and immune-mediated disease. In IgA nephropathy, bioinformatics analysis identified IL1B as one of six pyroptosis-related hub genes with high diagnostic accuracy, and the gene set was associated with immune response, cell migration, and inflammation-related pathways. In sickle cell disease, urinary IL-1β was proposed as an early biomarker for renal dysfunction and sickle nephropathy, reflecting interest in its potential to track early kidney injury. In periodontitis, a systematic review and meta-analysis found significantly elevated serum IL-1β in affected individuals, including in analyses restricted to systemically healthy participants, supporting its role in systemic inflammatory burden. Another periodontitis study identified IL1B+ macrophages as a pro-inflammatory subset and showed that targeting SERPINB9 with azilsartan medoxomil promoted apoptosis of these cells and alleviated alveolar bone loss.

Additional studies placed IL-1β within broader inflammatory and cell-death networks. In renal cancer stem cells, a nanoparticle-based ARDAP formulation induced PANoptosis and upregulated key pathway genes including Il1b, with ZFP148 shown to directly activate Il1b and other PANoptosis-related promoters. In vitiligo-related fibroblast injury, oxidative stress activated the cGAS-STING pathway and NLRP3 inflammasome, driving IL-1β expression as part of a senescence-associated secretory phenotype. In a study of sodium-glucose cotransporter-2 inhibitors, empagliflozin and dapagliflozin were evaluated for interactions with IL-1β among other targets, and both agents improved behavioral and biochemical measures in diabetic rats, with reduced brain IL-1β levels reported as part of the observed benefit.

Key Publications

May Neuroprotective effects of trans-anethole on AlCl₃-induced memory impairment: targeting AChE, oxidative stress, and NLRP3 inflammasome: a promising approach for neurodegeneration prevention. (Metabolic brain disease, 2026, PMID 42154340): "Neuroprotective effects were evaluated by analyzing acetylcholinesterase (AChE) activity, oxidative stress markers (catalase, glutathione, and malondialdehyde levels), and neuroinflammatory mediators (NLRP3 inflammasome, Interleukin-1β, and TNF-α) in AlCl₃-exposed rats."
Dec Identification of pyroptosis-related hub genes and immune cell infiltration in IgA nephropathy via bioinformatics analysis. (Renal failure, 2026, PMID 42135973): "A total of 19 pyroptosis-related differentially expressed genes (nine up-regulated and 10 down-regulated) were identified, with six hub genes (BHLHE40, JUN, CEBPB, ACE2, IL1B, and CD14) showing high diagnostic accuracy for discriminating IgAN from normal samples (AUC > 0.9)."
May Superparamagnetic iron oxide nanoparticle-driven 3-aroyl-1,4-diarylpyrrole nanocomposites (ARDAP@SPION-PEI) mediate renal cancer cell PANoptosis by regulating chromatin accessibility. (Molecular biomedicine, 2026, PMID 42138776): "Luciferase reporter assays demonstrated that ZFP148 directly bound to and activated promoters of key PANoptosis-related genes, including receptor-interacting serine/threonine kinase 3 (Ripk3), gasdermin D (Gsdmd), IL-1β (Il1b), and caspase-1 (Casp1)."
May The role of interleukin-1 beta as an early biomarker for renal dysfunction in Egyptian sickle cell disease patients. (Annals of hematology, 2026, PMID 42095901): "This study sought to investigate the relationship between urinary interleukin-1 beta (IL-1β), a marker of inflammation, and existing biomarkers of renal damage in SCD patients."
May Polystyrene nanoplastics induce hippocampal damage and cognitive deficits through oxidative stress-triggered microglial extracellular traps and neuronal ferroptosis. (Chemico-biological interactions, 2026, PMID 42070744): "This sustained neuroinflammatory response, characterized by the release of MiETs and increased levels of proinflammatory cytokines (Tumor Necrosis Factor-α (TNF-α) and Interleukin-1β (IL-1β)), was closely associated with neuronal ferroptosis."
Apr Systemic Cytokine Alterations in Periodontitis Independent of Comorbidities: A Systematic Review and Meta-Analysis. (Aging and disease, 2026, PMID 41910651): "analyses showed significantly (P<0.05) higher levels of C-C motif chemokine ligand 2 (CCL2); interleukin (IL)-1β, IL-6, IL-17, IL-17A and IL-18; leptin; matrix metalloproteinase 8 (MMP-8), myeloperoxidase (MPO); receptor activator of nuclear factor kappa-Β ligand (RANKL); and tumour necrosis factor α (TNF-α)."
May Repurposing Azilsartan medoxomil attenuates periodontitis by targeting SERPINB9 to promote apoptosis of IL1B+ macrophages. (International immunopharmacology, 2026, PMID 41864017): "Recent single-cell transcriptomic studies have identified IL1B+ macrophages as a pro-inflammatory subset closely linked to tissue destruction."
May Empagliflozin and dapagliflozin, sodium glucose cotransporter 2 inhibitors, may improve cognitive dysfunctions: in silico and in vivo findings. (Behavioural brain research, 2026, PMID 41819428): "...evaluating their in silico interactions with targets associated with oxidative stress, inflammation, and neuroprotection, including SGLT1, SGLT2, acetylcholinesterase (AChE), superoxide dismutase (SOD), receptor for advance glycation end-products (RAGE), and interleukin (IL)-1β."
Apr Targeting VDAC1-dependent mtDNA release attenuates fibroblast innate immune activation and vitiligo pathogenesis. (International immunopharmacology, 2026, PMID 41722540): "The released mtDNA activated the cGAS-STING pathway and the NLRP3 inflammasome, driving the expression of IL-1β, IL-6, ICAM-1, and Occludin-a pattern consistent with a senescence-associated secretory phenotype."
May Elucidating the effects of ginger processing on Magnolia bark: A multi-platform strategy linking chemical composition to taste and bioactivity. (Journal of pharmaceutical and biomedical analysis, 2026, PMID 41520497): "Network pharmacology identified 51 overlapping targets across FD, PONV, and CG, with AKT1, TNF, CTNNB1, IL1B, and STAT3 as core nodes in the network."