cytokine
IL-6
Inflammatory integrator linking acute phase response, fever, TH17 skewing, and metabolic stress
Review layer
Last reviewed 2026-05-17
Systems teaching draft. Content is structured for education and graph expansion, with formal source tagging ready for the next review pass.
Provenance layer
External context
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
System effects
Primary mapped axes from existing Atlas data.
Inflammation
Inflammatory alarm, recruitment, mediator release, or tissue-damaging amplification.
Metabolism
Energy allocation, glycolysis, mitochondrial strain, lipid signaling, or nutrient-sensitive behavior.
Neuroimmune
Nerve, neuropeptide, autonomic, microglial, pain, itch, fatigue, or sickness-behavior coupling.
Cascade viewer
Source → signal → tissue behavior
Sources
Signal
IL-6
Targets and effects
Graph neighborhood
Direct relationships
Arrow shows upstream source toward receiving target.
Acute phase and systemic inflammatory signaling
Context link: no causal arrow.
Neutrophil-rich inflammation often co-travels with IL-6 tone
Arrow shows upstream source toward receiving target.
IL-6 drives hepatic acute phase response
Context link: no causal arrow.
IL-6, cortisol rhythm, thyroid context, and metabolic stress interact in systemic inflammatory states
Cytokine ecology
Signal Role
IL-6 bridges innate inflammation, hepatic acute phase signaling, fatigue biology, and adaptive T cell differentiation.
Pathway
Source Cells
Target Cells
Inflammatory Role
Raises systemic inflammatory tone and supports acute phase proteins and TH17 conditions.
Regulatory Role
Can support tissue repair and B cell maturation when tightly time-limited.