“…19 In studies on mononuclear cells from patients with active RV the C3b and Fc receptors showed a defective ability to ingest and degrade soluble complexes of IgG in vitro. 3 Some patients with active joint disease and raised levels of CIC had similarly defective mononuclear cells. There is also some evidence indicating that immunogenetic factors can regulate the occurrence of certain aspects of systemic disease in patients with RA.202 More studies must be performed before it can be determined whether a group of RA patients with a high risk of developing clinical vasculitis can be defined prospectively by characteristics such as repeated demonstration of immune deposits in the papillary vessels of uninvolved skin, defective degradation of IC by mononuclear cells in vitro, and a HLA-DR4 phenotype.…”