Rheumatoid factors in subacute bacterial endocarditis and other infectious diseases.

Rheumatoid factors (RF) occur during the course of various infections such as leprosy, infective endocarditis, tuberculosis, trypanosomiasis, visceral larva migrans, infectious mononucleosis, influenza A, hepatitis A or cytomegalovirus. When first described it seemed logical to assume that host-self-immunization with autologous immune complexes provided the initial stimulus for RF production. Subsequently extensive characterization of bacterial, parasitic and viral Fc receptors has suggested an alternative explanation for rheumatoid factor associated with infections. It seems possible that patients make an initial immune response to infecting agent Fc receptors and that anti-anti-Fc receptors or anti-idiotypes either then directly stimulate rheumatoid factor production or are themselves rheumatoid factors. Such a hypothesis might also be applied to rheumatoid arthritis itself where either infecting agent or autologous cell Fc receptors could be the initial immunizing epitopes involved in rheumatoid factor production.