Rheumatoid Factor in Sjögren’s Syndrome

Abstract

Rheumatoid factors (RF) are defined by their ability to bind to the Fc portion of IgG molecules. This activity in the sera of rheumatoid arthritis (RA) patients was first noted as an atypical reaction during agglutination tests to detect antibodies to microbial antigens (Rose et al. 1948; Waaler 1940). The antibody nature of RF and its binding to different subclasses of IgG has been the subject of extensive investigations [reviewed in Fong et al. 1984]. As more sensitive tests for RF became available (Carson et al. 1977; Pope & McDuffy 1981; Koopman & Schrohenloher 1980), the presence of this antibody in other autoimmune conditions including Sjogren’s syndrome was recognized. Further, certain infectious diseases (Brouet et al. 1974) and B cell malignancies (Kunkel et al. 1961; Kunkel et al. 1973) are associated with RF. Recently, it has been recognized that this “autoantibody” may be synthesized in association with secondary immune responses in normal humans and in animals (Welch et al. 1983; Coulie & Van Snick 1983; Nemazee & Sato 1983). These results have suggested that RF plays a physiologic role in normal immune responses (Grabar 1983; Guilbert et al. 1983) and that persistent stimulation of these cells may lead to their neoplastic transformation (Berard et al. 1981).