Synonym(s)
Immunocomplex
DefinitionThis section has been translated automatically.
- Products of the antigen-antibody reaction. Small immune complexes are formed in the body on a daily basis, for example on contact with bacteria that enter the bloodstream in banal injuries and bind to antibodies there. This connection is also known to occur in viral infections. This is the case with hepatitis B and C (panarteriitis nodosa/hepatitis B, essential cryoglobulinemia/hepatitis C). The immune complexes are kept in soluble form by binding complement components. They bind to the complement receptor CR1 on erythrocytes and are transported to the liver where they are broken down.
- Large immune complexes with a tendency to deposit are formed when high, almost equimolar concentrations of antigens and antibodies meet. Antigens and antibodies then bind together and form large, strongly cross-linked immune complexes which are no longer soluble in plasma and precipitate (immunoprecipitation).
- In certain cases (see below autoimmune diseases) the immune complex also consists of autoantigen and autoantibodies (e.g. in SLE).
- The deposition of immune complexes in the vessels leads to complement activation and consecutive neutrophilic chemotaxis as well as to apoptotic decay of neutrophilic leukocytes (leukocytoclasia) (see below leukocytoclastic vasculitis; IgA nephropathy).
- Apparently, not only the deposition of circulating immune complexes from the blood is important for immune complex diseases, but also the in-situ formation after placement of an antigen or an antibody in the tissue itself (e.g. hepatitis C-AK in hepatitis C-infected keratinocytes). The classic representative of an immune complex disease is serum disease.
- The formation of large immune complexes is favoured in:
- Insufficient activation of the complement system (IgA, for example, is a weak activator of the classical complement system; see Purpura Schönlein-Henoch below)
- Lack of complement factors such as CR1,C1,C2,C4a (e.g. in the case of zero mutation of the gene)
- Degradation disorders of immune complexes.
- Deposition of circulating immune complexes on vessel walls is promoted by dilatation of the vessels, e.g. by stasis.
LiteratureThis section has been translated automatically.
- Fox MC et al (2008) Adult Henoch-Schönlein purpura in a patient with myelodysplastic syndrome and a history of follicular lymphoma. Cutis 81:131-137.
- Mao S et al (2015) Clinico-pathological association of Henoch-Schoenlein purpura nephritis and IgA nephropathy in children. Int J Clin Exp Pathol 8:2334-2342.
Prof. Dr. med. Peter Altmeyer