Abstract
It is now generally accepted that immune complexes play significant roles in the pathogenesis of rheumatoid arthritis. The complement must also respond to immune complexes and evidence in support of this has been accumulating. Membrane factors that control the complement system, e.g., DAF (decay accelerating factors), MCP (membrane cofactor protein), HRF (homologonous restriction factor) and HRF 20 (20 kDa homologonous restriction factor), have been reported. This study was undertaken to investigate the distribution of DAF in the peripheral blood lymphocyte subset involved in the pathogenetic mechanism of rheumatoid arthritis, i.e., CD8-positive cells (suppressor and killer cells), CD4-positive cells (helper and inducer cells) and CD19-positive cells (B cells) . The peripheral blood lymphocytes were investigated with two-color FACS-can analysis in 24 RA patients and 24 healthy controls.
The results indicated there to be a significant difference between the CD8-positive cells (suppressor/killer) of healthy individuals and those of RA patients in the proportion of DAF-positive cells. A significant difference was also observed between the two groups of subjects in the positive rate for DAF of CD4-positive cells (helper/inducer) . These differences were in favor of the controls. No significant difference was noted between the two groups with respect to CD19-positive cells (B cells) . The use or nonuse of corticosteroids made no significant difference in this regard. No correlation could be found between the positive rate for DAF of either of the CD8-positive cell subpopulations or the rheumatic disease activity index (Lansbury index) . The mechanism of the decreased expression of DAF on T lymphocytes of RA patients thus remains to be elucidated.
