A subpopulation of lymphocytes detected by the use of calf erythrocytes sensitized with the Facb fragment of rabbit immunoglobulin G (lgG) were compared in healthy control subjects and in patients with rheumatoid arthritis. These cells (Facb R+ cells) were found to be less dense in rheumatoid patients than in controls. They were also found to be steroid sensitive in the former group but not in the latter. Electron micrographs indicated that Facb R+ cells in patients with RA were metabo1ically more active than in normal controls. It was found that a transient increase in the number of circulating Facb R+ cells could be induced in control subjects by antigenic challenge. Studies in mice showed that an increase in %Facb R+ splenic lymphocytes could be induced by antigenic challenge in sensitized animals. Experiments involving the adoptive transfer of sensitized cells showed that the Facb R+ cell is involved in suppression of Ig synthesis. This suppression was shown to require interaction between IgG and the Fc receptor on Facb R+ cells. Similar results were obtained in experiments using human cells. These results are discussed in relation to current concepts of Fc-mediated suppression of humoral immunity. A longitudinal study of patients with early rheumatoid disease showed that the %Facb R+ peripheral blood lymphocytes correlated with the clinical assessment of disease activity. This correlation was lost in patients with established RA receiving D-Penicillamine therapy. The implications of these results are discussed in relation to observations made on the in vitro effect of thiol containing compounds on the expression of Fc receptors on Facb R+ cells.
|Date of Award||1982|