IMMUNE OS ATLASby AllerimSign in

clinical pattern

Inflammasome Pattern

IL-1beta, macrophage priming, danger sensing, and metabolic stress

IL-1betamacrophageNLRP3metabolic stress

Review layer

Last reviewed 2026-05-17

well-supportedclinical context required

Use as a conceptual pattern for innate danger sensing, metabolic stress, and IL-1beta-rich inflammatory states.

3 review sources

Provenance layer

External context

static reviewed map

Curated external IDs add pathway and protein context around Atlas content. They do not update the graph automatically and they are not patient-specific interpretation.

State signature

Systems profile

Inflammation86
Tolerance45
Metabolism82
Tissue62
Neuroimmune80
Chronicity78

System effects

Primary mapped axes from existing Atlas data.

Interpretive

Inflammation

High 86

Inflammatory alarm, recruitment, mediator release, or tissue-damaging amplification.

IL-1betaIL-6TNF-alphaCRP

Metabolism

High 82

Energy allocation, glycolysis, mitochondrial strain, lipid signaling, or nutrient-sensitive behavior.

No direct axis cue is mapped for this node yet.

Neuroimmune

High 80

Nerve, neuropeptide, autonomic, microglial, pain, itch, fatigue, or sickness-behavior coupling.

No direct axis cue is mapped for this node yet.

Pattern signature

Recognizable immune constellation

Signals

01

IL-1beta

IL-6

TNF-alpha

CRP

ROS

Cells

02

macrophages

neutrophils

monocytes

Tissues

03

adipose

liver

gut

vasculature

Restraint

04

IL-10

AMPK

autophagy

efferocytosis

resolvins

Graph neighborhood

Direct relationships

Full graph

Context link: no causal arrow.

Danger sensing and IL-1 family activation

Context link: no causal arrow.

Signature inflammasome output

Pattern logic

Interpretation

Map the trigger source: microbial products, urate/cholesterol crystals, hypoxia, mitochondrial injury, or chronic lipid overload.

Dominant Signals

Dominant Cells

macrophagesneutrophilsmonocytes

Tissue Context

adiposelivergutvasculature

Counter Regulation

IL-10AMPKautophagyefferocytosisresolvins