inflammation
Immune-complex formation and clearance
Immune complexes are not automatically disease. They become important when their size, solubility, antibody class, complement fixation, tissue location, and clearance capacity change inflammatory consequences.
Provenance layer
Pathway provenance 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.
Complement cascade
R-HSA-166658 · parent pathway
Complement and immune-complex clearance context; not a diagnostic rule.
Last checked 2026-06-28
Complement C1q subcomponent subunit A
P02745 · protein
Reviewed C1QA protein identity anchor for classical complement context.
Last checked 2026-06-28
Pathway logic
Trigger to state transition
Immune-complex biology explains clearance and amplification; it should not be used as a broad diagnosis without a clinical context.
Entry triggers
Key signals
Labs and data
Visual sequence
formation
Antigen plus antibody
Complexes form when antibodies bind soluble or particulate antigen. Size, valency, and class matter.
reading
Complement and Fc receptor reading
C1q, complement fragments, Fc receptors, and phagocytes translate complexes into clearance or inflammation.
clearance
Liver, spleen, and macrophage clearance
Clearance systems normally remove complexes and prevent tissue deposition.
injury
Deposition or inflammatory amplification
When complexes persist or deposit, complement and neutrophil recruitment can create tissue injury.
Cells
macrophages
neutrophils
B cells
plasma cells
endothelial cells
Tissues
vasculature
kidney/skin/joint contexts
liver
spleen
Caveats
Immune complexes are common and often cleared normally.
Complement labs are context-dependent.
Deposition disease requires clinical evaluation.
Cross-links