ANTI-DSDNA PRODUCTION COINCIDES WITH CONCURRENT B-CELL AND T-CELL ACTIVATION DURING DEVELOPMENT OF ACTIVE DISEASE IN SYSTEMIC LUPUS-ERYTHEMATOSUS (SLE)

The objective was to serially analyse T and B cell activation in relat ion to autoantibody production during the development of relapses in S LE. In a prospective study we serially analysed, by flow cytometry, T cell activation to B cell activation and anti-dsDNA production in quie scent SLE and during the development of a clinical relapse. In additio n, we related changes in T and B cell activation to changes in levels of anti-dsDNA and total IgG. During periods with clinically quiescent disease, the expression of activation markers on T cells (IL-2R and HL A-DR) and B cells (CD38) was persistently higher in SLE than in health y controls (P < 0.001). Percentages of CD20(+)CD38(+) B cells were rel ated to levels of total IgG (P < 0.02), but not to levels of anti-dsDN A. Development of disease activity was paralleled by an increase in th e percentages of CD4(+) T cells (P < 0.005) and CD20(+)CD38(+) B cells (P < 0.001), which were interrelated. Increases in B cell activation were related to increases in levels of anti-dsDNA (P < 0.005), but not to changes in total IgG levels. B cells expressing high levels of CD3 8 spontaneously produced IgG class anti-dsDNA in vitro. Persistence of activated B cells during periods with clinically quiescent disease in SLE seems to underly hypergammaglobulinaemia but not anti-dsDNA produ ction. Prior to clinical disease activity, further activation of T and B cells occurs, which is paralleled by rises of anti-dsDNA but not of total IgG. This suggests that the production of anti-dsDNA is a T cel l-dependent antigen-driven process, which is independent of the polycl onal activation of the immune system inherent to the disease.