The first thought is –> remove the complexes; this will have transient therapeutic efficacy only because the underlying causes of formation of immune complexes continue their activity. Knowing the triggering antigen means targeting therapy to the root.
If antigen an infectious agent, then anti-infectious therapy is the center core of any approach, even when –> vasculitis, arthritis, proteinuria or peripheral blood cytopenia are complicating.
In patients with high levels of IC, sometimes revealing cryoglobulins –> plasma exchange therapy as palliative measure but this must be adjuvant to overall therapeutic concept avoiding re-build of IC.
Now knowing the involved antigen in IC the therapeutic schemes are inspired from treatment strategies used in autoimmune diseases: corticosteroids, aspirin derivatives (azulfidine), mild immunosuppressants (chloroquine, methotrexate), cytostatics (azathioprin) and mAbs. Too early to speculate on the impact of the crispr/Cas9 possibility to modulate autoimmune diseases –> more news after april 2016 coming home from Leipzig April in Leipzig 2016
The second thought is make complexes innocuous! Treatment with endoglycosidases (EndoS) secreted by streptococci remove the capacities of IC to bind to FcR and complement thus mitigating pathogenic power (www.genovis.com) –> under study for its suitability to clinical application.