01759nas a2200265   4500000000100000008004100001260000900042653003100051653002300082653002500105653003700130653001100167653002900178653002300207653002300230653001800253653002200271653001900293100001700312245008900329300001000418490000700428520104400435022001401479       1988                            d  c198810aAntibodies, Anti-Idiotypic10aAntibody Formation10aBacterial Infections10aEndocarditis, Subacute Bacterial10aHumans10aImmunoglobulin Idiotypes10aModels, Biological10aParasitic Diseases10aReceptors, Fc10aRheumatoid Factor10aVirus Diseases1 aWilliams R C00aRheumatoid factors in subacute bacterial endocarditis and other infectious diseases.  a300-80 v753 a<p>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.</p>  a0301-3847