- published a "Current Comment"' in Arthritis and Rheumatism concerning the "C3b receptor (CR1) deficiency" of red blood cells (RBC) in systemic lupus erythematosus (2-6) and in some other immune complex-mediated diseases (4,6,7). However, if this "relative deficiency" is well-documented, one question that remains open to discussion concerns its inherited (2,3,5) or acquired (4,6) origin. Since in the paper by Wilson and Fearom, no mention was made of the eventual relationships between the CRl-RBC status and the H L A phenotype, we would like to present some aspects of a study analyzing these latter parameters.
One hundred fifty men and women entered this study. Of these, 110 had chronic renal failure secondary to either glomerulonephritis (38 patients), pyelonephritis (44 patients), phenacetin-induced tubulointerstitial nephritis (20 patients), or polycystic kidneys (8 patients) and were being treated by iterative hemodialysis; 20 presented with classic rheumatoid arthritis (RA); and 20 were control subjects. The CR1 expression of the RBCs was measured according to radioligand binding assays (5,8), using saturating amounts of both anti-CRl monoclonal antibody (Dakopatts, Copenhagen, Denmark) and goat anti-mouse IgG (Tago, Burlingame, CA), labeled with 1251. The DR phenotypes were determined