Immune Complex Diseases A distinct collection of diseases characterized by immune complexes causing and entertaining the disease process can be delineated. Desoxyribonucleic acid, DNA, is the predominant antigen in complexes found in systemic lupus erythematosus, and IgG itself is found in rheumatoid arthritis. Anti-citrullinated protein antibodies react to entirely different target antigens; citrullinated peptides or arginine-containing cellular proteins are involved.
The seropositive forms of ankylosing spondylitis and Wegeners granulomatosis fall in the same category without displaying distinct antigen specificity. Infectious diseases, with which the host fails to remove the infectious antigen –> chronic immune complex diseases
e.g. Mycoplasma pneumoniae, Hepatitis, Dengue fever, Toxoplasma; Zika does not list.
Diabetic nephropathy is aggravated by NLRP3-inflammasome inducing IL-1beta;
If immune complexes suppress IL1beta, then their presence in nephropathy would
be welcome in this respect: research to follow as of 2017.
Some renal diseases, i.e. IgA nephropathy and Membranous proliferative glomerulonephritis feature lobular accentuation of glomerular tufts from deposition of ICs, Complement factors in glomerular mesangium and along glomerular capillary walls. Immunohematological diseases (immune haemolytic anemia, immune thrombocytopenia) and iatrogenic diseases (gold nephropathy, acute serum sickness with antilymphocyte globulin) –> immune complexes involved.
Common denominator of all these diseases: systemic or local damage due to immune complexes; distictive features: the predominance of organ deposition/damage which differs and gives the entities their names; G-CSF is a driver of organ damage induced by immune complexes. Both types of immune complexes exist: those which activate complement to cause damage and those who are damped thanks to complement activation, if both events do not occur jointly –> bidirectional feedback loops.