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.

Recent Publications Focus

Below is a summary of the newest research publications targeting Interleukin 1 beta (sorted by publication date).

Recent studies have continued to place Interleukin 1 beta (IL1B) within broader inflammatory and neuroimmune networks. In an Alzheimer's disease-focused network pharmacology and molecular docking analysis, IL1B emerged as one of 14 key overlapping targets linking gut microbiota-derived metabolites to immune-inflammatory pathways, alongside IL6, NFKB1, TLR4, PPARG, and PTGS2. The study associated these targets with immune-inflammatory responses, oxidative stress, apoptosis regulation, and signaling pathways including NOD-like receptor, TNF, NF-κB, and MAPK. In the same publication, selected metabolites such as Enterodiol and Coumarin were docked against representative hub proteins, but the docking results were presented only as qualitative structural compatibility rather than evidence of biological activity.

Several experimental studies also examined IL1B in neuroinflammation and cognitive dysfunction. In an aluminum-induced rat model of memory impairment, trans-anethole reduced neurodegeneration-associated changes and downregulated inflammatory mediators including NLRP3, TNF-α, and IL-1β, alongside improvements in antioxidant defenses and acetylcholinesterase activity. Similarly, in mice exposed to polystyrene nanoplastics, hippocampal oxidative stress activated microglia and promoted microglial extracellular traps, with increased TNF-α and IL-1β linked to neuronal ferroptosis and cognitive deficits; N-acetylcysteine attenuated these effects. Another study in type 2 diabetes-associated cognitive dysfunction evaluated empagliflozin and dapagliflozin in silico and in vivo, including IL-1β among the inflammatory and neuroprotective targets assessed in brain tissue, with treatment associated with improved behavioral performance and biochemical markers.

IL1B has also been highlighted in renal and immune-mediated disease contexts. In IgA nephropathy, bioinformatics analysis identified IL1B as one of six pyroptosis-related hub genes with high diagnostic accuracy, and pathway analysis implicated immune response, cell migration, and inflammation-related signaling. In sickle cell disease, urinary IL-1β was investigated as a potential early biomarker of renal dysfunction and sickle nephropathy. In periodontitis, a systematic review and meta-analysis found serum IL-1β significantly elevated compared with controls, including in analyses restricted to systemically healthy participants, supporting its role in systemic inflammatory burden. A separate periodontitis study focused on IL1B+ macrophages and identified SERPINB9 as a key regulator of macrophage survival; pharmacological inhibition of SERPINB9 reduced inflammatory macrophage responses and alveolar bone loss.

Additional publications linked IL1B to cell death programs and inflammatory signaling in other disease models. In renal cancer stem cells, ARDAP@SPION-PEI induced PANoptosis and upregulated key pathway genes, with ZFP148 directly activating promoters of Ripk3, Gsdmd, Il1b, and CASP1. In vitiligo, oxidative stress triggered VDAC1-dependent mitochondrial DNA release, activating cGAS-STING and NLRP3 inflammasome signaling and increasing IL-1β expression in dermal fibroblasts. Across these studies, IL1B repeatedly appeared as a central inflammatory mediator connected to pyroptosis, inflammasome activation, oxidative stress, and tissue injury, making it a recurring target in hypothesis-generating work across neurodegenerative, renal, oral, dermatologic, and cancer-related research.

Background PMIDs

• [PMID 41732673]

Method PMIDs

• [PMID 42033182]
• [PMID 42144021]
• [PMID 42168453]
• [PMID 42213222]
• [PMID 42392495]

Result PMIDs

• [PMID 41512601]
• [PMID 41628818]
• [PMID 41638470]
• [PMID 41663028]
• [PMID 41734874]
• [PMID 41864015]
• [PMID 41935781]
• [PMID 41937019]
• [PMID 41941975]
• [PMID 41997405]
• [PMID 42002091]
• [PMID 42003370]
• [PMID 42025655]
• [PMID 42049099]
• [PMID 42059452]
• [PMID 42119768]
• [PMID 42133132]
• [PMID 42142128]
• [PMID 42154095]
• [PMID 42174225]
• [PMID 42217656]
• [PMID 42324965]
• [PMID 42388654]
• [PMID 42390648]
• [PMID 42396641]
• [PMID 42396648]
• [PMID 42401089]

Target PMIDs

• [PMID 41520497]
• [PMID 41722540]
• [PMID 41819428]
• [PMID 41864017]
• [PMID 41910651]
• [PMID 42070744]
• [PMID 42095901]
• [PMID 42135973]
• [PMID 42138776]
• [PMID 42154340]
• [PMID 42406869]

Conclusion PMIDs

• [PMID 41934393]