protein

IL-1Β

Entity Detail — Knowledge Graph Node

Understanding Entity Pages

This page aggregates everything SciDEX knows about IL-1Β: its mechanistic relationships (Knowledge Graph edges), hypotheses targeting it, analyses mentioning it, and supporting scientific papers. The interactive graph below shows its immediate neighbors. All content is AI-synthesized from peer-reviewed literature.

396Connections

9Hypotheses

14Analyses

50Outgoing

50Incoming

1Experiments

20Debates

Summary

Page for IL-1β Protein

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🔬 Protein Info

Gene Symbol	IL
Function	Interleukin-1 beta (IL-1β) is a potent pro-inflammatory cytokine that plays a central role in the innate immune response and neuroinflammation.
GeneCards	IL
Human Protein Atlas	IL
Associated Diseases	CRC
KG Connections	1 knowledge graph edges
Databases	GeneCards UniProt NCBI Gene HPA STRING

Pathway Diagram

graph TD
    IL_1_["IL-1Beta"]
    Parkinson_s_Disease{"Parkinson's Disease"}
    IL_1_ -->|"biomarker_for"| Parkinson_s_Disease
    Neuroinflammation["Neuroinflammation"]
    IL_1_ -->|"contributes_to"| Neuroinflammation
    Liver_Fibrosis{"Liver Fibrosis"}
    IL_1_ -->|"contributes_to"| Liver_Fibrosis
    Neurodegeneration["Neurodegeneration"]
    IL_1_ -->|"biomarker_for"| Neurodegeneration
    Hepatic_Stellate_Cell_Activati["Hepatic Stellate Cell Activation"]
    IL_1_ -->|"associated_with"| Hepatic_Stellate_Cell_Activati
    Spinal_Cord_Injury_Inflammatio["Spinal Cord Injury Inflammation"]
    IL_1_ -->|"mediates"| Spinal_Cord_Injury_Inflammatio
    NLRP3_INFLAMMASOME(["NLRP3 INFLAMMASOME"])
    NLRP3_INFLAMMASOME -->|"associated_with"| IL_1_
    Ua["Ua"]
    Ua -.->|"downregulates"| IL_1_
    NLRP3["NLRP3"]
    NLRP3 -->|"activates"| IL_1_
    NLRP3_Inflammasome_Activation["NLRP3 Inflammasome Activation"]
    NLRP3_Inflammasome_Activation -->|"associated_with"| IL_1_
    style IL_1_ fill:#1a3a4a,stroke:#4fc3f7,stroke-width:3px,color:#4fc3f7

Outgoing (222)

Target	Relation	Type	Str
Neuroinflammation	contributes_to	process	0.95
Innate Immune Memory	associated_with	process	0.95
Neuroinflammation	mediates	process	0.90
Chondrocyte Viability	inhibits	phenotype	0.90
ST6GAL1	contributes_to	gene	0.90
NF-kB	activates	protein	0.90
Alzheimer's_disease	associated_with	disease	0.90
INFLAMMATION	promotes	process	0.90
NEURON	associated_with	cell_type	0.90
complement cascade upregulation	causes	process	0.90
spine loss	causes	phenotype	0.90
neurotoxic inflammation	causes	mechanism	0.90
p25/CDK5 pathway	activates	pathway	0.90
NLRP3	activates	protein	0.90
tau phosphorylation	causes	mechanism	0.90
Epigenetic Changes	modulates	mechanism	0.89
Synaptic Dysfunction	causes	process	0.88
Traumatic Brain Injury	biomarker_for	disease	0.85
Liver Fibrosis	contributes_to	disease	0.85
Neuroinflammation	mediates	process	0.85
Parkinson's Disease	biomarker_for	disease	0.85
Myeloid Cell Immune Response	mediates	process	0.85
Neurodegeneration	promotes	phenotype	0.85
Ulcerative Colitis	biomarker_for	disease	0.85
Pro-Inflammatory Phenotype	associated_with	phenotype	0.85
Neuroinflammation	contributes_to	process	0.85
Ovary Inflammation	promotes	process	0.85
Neurodegeneration	biomarker_for	process	0.82
Status Epilepticus	biomarker_for	disease	0.80
Alzheimer's Disease	contributes_to	disease	0.80
neuroprotective effects of Quercetin	inhibits	process	0.80
innate immune memory	drives	process	0.80
STROKE	promotes	disease	0.80
neurons	damages	cell_type	0.80
H2S	upregulates	compound	0.80
Hepatic Stellate Cell Activation	associated_with	process	0.80
Neuroinflammation	promotes	process	0.80
Spinal Cord Injury Inflammation	mediates	process	0.80
tau release	causes	phenotype	0.70
epilepsy	associated_with	disease	0.70
C3 expression	activates	phenotype	0.70
microglial complement expression	regulates	phenotype	0.70
neuronal tau phosphorylation	causes	phenotype	0.70
IL1R1/MYD88 signaling	activates	pathway	0.70
M1 pro-inflammatory phenotype	biomarker_for	cell_type	0.70
Microglial complement expression	regulates	phenotype	0.70
Bbb Disruption	causes	phenotype	0.70
C3	upregulates	gene	0.70
microglial activation	causes	process	0.70
NfL elevation	associated_with	biomarker	0.70

Incoming (174)

Source	Relation	Type	Str
secretory autophagy	regulates	process	0.95
NLRP3	upstream_of	protein	0.95
Berberine	inhibits	compound	0.95
HSYA	downregulates	compound	0.95
Fingolimod	downregulates	drug	0.92
Cerebral Ischemia-Reperfusion Injury	upregulates	disease	0.92
NLRP3	regulates	gene	0.90
NLRP3	produces	protein	0.90
miR-369-3p	downregulates	biomarker	0.90
Anakinra	inhibits	drug	0.90
DHT	downregulates	compound	0.90
Gallic Acid	downregulates	compound	0.90
NLRP3 Inflammasome Activation	activates	process	0.90
NLRP3	activates	gene	0.90
NLRP3 INFLAMMASOME	associated_with	protein	0.90
NLRP3	activates	entity	0.90
NLRP3	upregulates	protein	0.90
Ua	downregulates	compound	0.90
TLR4	upregulates	protein	0.90
NLRP3	upregulates	protein	0.90
37245027	induces reduction of	paper	0.90
37245027	induces	paper	0.90
PS-COOH	upregulates	compound	0.90
NLRP3 Inflammasome Activation	associated_with	process	0.90
pyroptosis	promotes	process	0.90
canakinumab	inhibits	drug	0.90
Bergenin	downregulates	compound	0.90
NLRP3 Inflammasome	associated_with	mechanism	0.90
DS-HMGB1	upregulates	protein	0.90
32505187	was increased in	paper	0.90
Indirubin	downregulates	compound	0.90
Ciprofloxacin	downregulates	drug	0.90
Microglia	produces	cell_type	0.90
CASP1	activates	protein	0.90
NF-κB	upregulates	pathway	0.88
NLRP3 Inflammasome	upregulates	mechanism	0.88
cGAS-STING	upregulates	pathway	0.85
NLRP3	regulates	protein	0.85
Palmitoleic Acid	downregulates	compound	0.85
MIR-369-3P	downregulates	gene	0.85
BIG1	upregulates	gene	0.85
Nf-Κb	regulates	protein	0.85
Guhan Yangsheng Jing	downregulates	drug	0.85
IL-17 Signaling Pathway	upregulates	pathway	0.85
Ischemia	upregulates	disease	0.85
Rutin	downregulates	compound	0.85
NF-κB	regulates	protein	0.85
S1PR1	promotes	protein	0.85
NF-κB signaling pathway	upstream_of	pathway	0.85
NLRP3	activates	gene	0.80

Targeting Hypotheses (9)

Hypotheses where this entity is a therapeutic target

Hypothesis	Score	Disease	Analysis
TNF-α/IL-1β-Cx43 Hemichannel Axis as Upstream Link Between S	0.663	cell biology	What is the relative contribution of con
Astrocyte IL-1β as Paracrine Mediator of Microglial Compleme	0.658	neuroinflammation	How does sevoflurane-induced NF-κB activ
NLRP3 Inflammasome Priming Converts SCFA-Sensitive Pyroptosi	0.620	neurodegeneration	How does gut microbiome dysbiosis contri
LRP1/NLRP3/IL-1β Cascade Links Aβ Endocytosis to Inflammasom	0.617	neurodegeneration	How do perivascular cells specifically r
NLRP3 Inflammasome Inhibition Prevents Synapse Loss via IL-1	0.610	neurodegeneration	Test Preregistration Analysis

Circulating hs-CRP as Disease-Modifying Target via Microglia	0.565	immunomics	Systemic immune profiling in neurodegene
TYRO3-STAT1 Axis to Preserve Parvalbumin Interneuron Functio	0.506	neuroinflammation	Why do TAM receptors protect against neu
CRP-Mediated CCR2+ Monocyte Recruitment Drives Microglial IL	0.380	immunomics	Systemic immune profiling in neurodegene
hs-CRP-Driven CCR2+ Monocyte Recruitment Disrupts CNS Immune	0.357	immunomics	Systemic immune profiling in neurodegene

Mentioning Analyses (14)

Scientific analyses that reference this entity

Test Preregistration Analysis

neurodegeneration | 2026-04-27 | 7 hypotheses Top: 0.710

Neuroinflammation Biomarker Panel for Early AD Detection

neurodegeneration | 2026-04-18 | 7 hypotheses Top: 0.105

Analyze the spectrum of microglial activation states (DAM, homeostatic, inflamma

neurodegeneration | 2026-04-17 | 0 hypotheses

Systemic immune profiling in neurodegeneration: peripheral inflammation as drive

immunomics | 2026-04-16 | 13 hypotheses Top: 0.565

Does APOE4 drive tau propagation

neurodegeneration | 2026-04-15 | 0 hypotheses

Experiments (1)

Experimental studies targeting or related to this entity

Experiment	Type	Disease	Score	Feasibility	Model	Status	Est. Cost
Network pharmacology analysis of QTJD active compounds and pathways	exploratory	Mycoplasma pneumoniae pneumoni	0.900	0.00	computational network analysis	proposed	N/A

Related Papers (0)

Scientific publications cited in analyses involving this entity

Title & PMID	Authors	Journal	Year	Citations
No papers found

Debates (20)

Multi-agent debates referencing this entity

Test question for preregistration

active · Rounds: 4 · Score: 0.77 · 2026-04-28

Extended debate: Metabolic Reprogramming to Reverse Senescence

closed · Rounds: 6 · Score: 0.95 · 2026-04-27

Hypothesis debate: Metabolic Reprogramming to Reverse Senescence

closed · Rounds: 4 · Score: 0.44 · 2026-04-27

Hypothesis debate: SASP Modulation Rather Than Cell Elimination

closed · Rounds: 4 · Score: 0.50 · 2026-04-26

Hypothesis debate: Metabolic Reprogramming to Reverse Senescence

closed · Rounds: 4 · Score: 0.50 · 2026-04-26

Hypothesis debate: Metabolic Reprogramming to Reverse Senescence

closed · Rounds: 4 · Score: 0.50 · 2026-04-26

Should metabolic reprogramming via SIRT1/NAD+/PGC-1alpha axis be prioritized to

closed · Rounds: 4 · Score: 0.81 · 2026-04-23

Investigate mechanisms of epigenetic reprogramming in aging neurons

closed · Rounds: 4 · Score: 0.79 · 2026-04-22

The abstract indicates SPP1 upregulation occurs in perivascular macrophages and

closed · Rounds: 4 · Score: 0.67 · 2026-04-22

The abstract identifies APOE4 association with increased TDP-43 pathology but th

closed · Rounds: 4 · Score: 0.61 · 2026-04-21

Related Research

Hypotheses and analyses mentioning IL-1Β in their description or question text

Circulating hs-CRP as Disease-Modifying Target via Microglial IL-1β Amplificatio

Score: 0.565 · immunomics · 2026-04-25

Circulating hs-CRP as Disease-Modifying Target via Microglial IL-1β Amplification

TYRO3-STAT1 Axis to Preserve Parvalbumin Interneuron Function by Suppressing IL-

Score: 0.506 · neuroinflammation · 2026-04-14

## Mechanistic Overview TYRO3-STAT1 Axis to Preserve Parvalbumin Interneuron Function by Suppressing IL-1β-Mediated Infl

CRP-Mediated CCR2+ Monocyte Recruitment Drives Microglial IL-1β Amplification an

Score: 0.380 · immunomics · 2026-04-27

This hypothesis proposes that circulating hs-CRP directly recruits CCR2+ monocytes to the CNS through upregulation of CC

hs-CRP-Driven CCR2+ Monocyte Recruitment Disrupts CNS Immune Privilege via IL-1β

Score: 0.357 · immunomics · 2026-04-26

Circulating hs-CRP directly triggers CCR2+ monocyte recruitment to the CNS by enhancing CCL2 expression in brain endothe

IL-1Β

Understanding Entity Pages

Summary

Pathway Diagram

Outgoing (222)

Incoming (174)

Targeting Hypotheses (9)

Mentioning Analyses (14)

Test Preregistration Analysis

Neuroinflammation Biomarker Panel for Early AD Detection

Analyze the spectrum of microglial activation states (DAM, homeostatic, inflamma

Systemic immune profiling in neurodegeneration: peripheral inflammation as drive

Does APOE4 drive tau propagation

Why do TAM receptors protect against neuroinvasive viruses despite their known i

Do SPM receptors undergo desensitization with chronic agonist treatment, prevent

How does sevoflurane-induced NF-κB activation specifically trigger complement ca

What causes IBA1 low/negative microglia in liver disease and how does this affec

How does APOE4 mechanistically increase TDP-43 pathology frequency in Alzheimer'

How do perivascular cells specifically recognize and respond to amyloid-β to upr

Investigate mechanisms of epigenetic reprogramming in aging neurons

Neuroinflammation and microglial priming in early Alzheimer's Disease

Senescent cell clearance as neurodegeneration therapy

Experiments (1)

Related Papers (0)

Debates (20)

Test question for preregistration

Extended debate: Metabolic Reprogramming to Reverse Senescence

Hypothesis debate: Metabolic Reprogramming to Reverse Senescence

Hypothesis debate: SASP Modulation Rather Than Cell Elimination

Hypothesis debate: Metabolic Reprogramming to Reverse Senescence

Hypothesis debate: Metabolic Reprogramming to Reverse Senescence

Should metabolic reprogramming via SIRT1/NAD+/PGC-1alpha axis be prioritized to

Investigate mechanisms of epigenetic reprogramming in aging neurons

The abstract indicates SPP1 upregulation occurs in perivascular macrophages and

The abstract identifies APOE4 association with increased TDP-43 pathology but th

Related Research

Circulating hs-CRP as Disease-Modifying Target via Microglial IL-1β Amplificatio

TYRO3-STAT1 Axis to Preserve Parvalbumin Interneuron Function by Suppressing IL-

CRP-Mediated CCR2+ Monocyte Recruitment Drives Microglial IL-1β Amplification an

hs-CRP-Driven CCR2+ Monocyte Recruitment Disrupts CNS Immune Privilege via IL-1β