Immune-complexes can become mischief-makers if their appearance is temporally not limited, i.e. followed by elimination of antigen and/or allow the (auto-)antigen go to its rest. In such case, they induce inflammation.
By its own, inflammation is a localized protective tissue response elicited by injury, destruction or immune-complex deposition, which serves to destroy, dilute, or wall off (sequester) both the injurious agent and the injured tissue. It is characterized in the acute form by the classical signs of dolor, calor), rubor, tumor, and functio laesa. The inflammasome protein complex mediates inflammation arousal.
Histologically it involves serial steps, including dilatation of arterioles, capillaries, and venules, with increased permeability and blood flow; exudation of fluids, including plasma proteins; and leukocytic migration into the inflammatory focus.
Immune-complex induced inflammation may remain localized (successful containment) or become systemic thus encompassing the whole body, e.g. with local immune-complex deposits i.e. as with vasculitis, arthritis or with debilitating febrile consequences. TNF-like ligand 1A (TL1A) and its interaction with death receptor 3 (DR3) is critically involved in the pathogenesis of autoimmune diseases – immune complexes, among other factors, triggering recruitment.
NOD-like receptors (NLRs) sense danger signals and form large cytoplasmic complexes: inflammasomes: these sense microbial products and metabolic stress which is followed by IL-1 and IL-18 activation.
Our recent paper on this topic is linked here
update july 2017