Immune system ↗PAMPs and DAMPs reveal disruption
Microbial patterns, cell injury, crystals, toxins, foreign material, and mechanical damage engage different sensors and tissue compartments.
IMMUNE / 05
Start enough.
Stop on time.
Inflammation is a coordinated tissue response to infection, injury, or disturbance. Successful defense requires initiation, amplification, containment, active resolution, and repair—not permanent suppression.
Resident cells set the first response
Macrophages, mast cells, dendritic cells, epithelium, endothelium, and nerves release a context-dependent combination of mediators.
Blood delivery is locally redirected
Vasodilation increases flow; permeability moves proteins and fluid; adhesion molecules slow and capture circulating leukocytes.
Gradients guide cell entry
Chemokines, complement fragments, lipid mediators, and microbial products direct neutrophils and monocytes across vessel and matrix.
Rapid killing carries collateral risk
Phagocytosis, granules, oxidants, proteases, and extracellular traps can contain threats while also damaging nearby host structures.
Clearance and coordination overlap
Macrophages ingest microbes and debris, present antigen, produce cytokines, recruit other cells, and interpret repair signals.
Local clotting helps contain injury
Platelets, fibrin, endothelium, complement, and innate signals interact to seal damaged vessels and restrict spread.
Brakes appear during activation
Inhibitory receptors, receptor desensitization, regulatory cytokines, short mediator half-lives, and anti-proteases constrain injury.
Control requires less incoming danger
Microbial killing, source control, toxin removal, sealing of the barrier, and debris clearance reduce continued stimulation.
New neutrophil entry declines
Changing chemokines, endothelial signals, lipid mediators, and trigger burden reduce further tissue infiltration.
Short-lived effectors shut down
Spent neutrophils undergo controlled cell death that packages damaging contents and exposes signals for phagocytic clearance.
Macrophages clear dying cells
Engulfment prevents secondary necrosis and changes macrophage output toward anti-inflammatory and repair-supporting programs.
Stopping is actively instructed
Lipoxins, resolvins, protectins, maresins, annexin pathways, IL-10, TGF-β, and neuronal inputs participate in context-dependent resolution.
Cells leave, die, or become resident
Leukocytes may exit through lymph, die locally, recirculate, or adopt tissue-supportive states as structure is restored.
Persistent activation changes tissue
Ongoing trigger, poor clearance, repeated injury, impaired perfusion, metabolic stress, or regulatory failure can produce chronic inflammation and fibrosis.