Complement receptor 1 (CD35) on human reticulocytes: Normal expression in systemic lupus erythematosus and HIV-infected patients

The low levels of complement receptor 1 (CR1) on erythrocytes in autoimmune diseases and AIDS may be due to accelerated loss in the circulation, or to a diminished expression of CRI on the red cell lineage. Therefore, we anal yzed the expression of CRI on reticulocytes (R) vs erythrocytes (E), Health y subjects had a significant higher CR1 number per cell on R (919 +/- 99 CR 1/cell) than on E (279 +/- 30 CR1/cell, n = 23), which corresponded to a 3. 5- +/- 1.3-fold loss of CR1, This intravascular loss was confirmed by FAGS analysis, which showed that all R expressed CR1, whereas a large fraction o f E was negative, The systemic lupus erythematosus (SLE), HIV-infected, and cold hemolytic Ab disease (CHAD) patients had a CR1 number on R identical to the healthy subjects, contrasting with a lower CR1 on their E, The data indicated a significantly higher loss of CR1 in the three diseases, i.e., 7 .0- +/- 3.8-, 6.1- +/- 2.9-, and 9.6- +/- 5.6-fold, respectively, The intra vascular loss was best exemplified in a patient with factor I deficiency wh ose CR1 dropped from 520 CR1/R to 28 CR1/E, i.e., 18.6-fold loss. In one SL E patient and in the factor I-deficient patient, the FAGS data were consist ent with a loss of CR1 already on some R. In conclusion; CR1 is lost progre ssively from normal E during in vivo aging so that old E are almost devoid of CR1, The low CR1 of RBC in autoimmune diseases and HIV-infection is due to a loss occurring in the circulation by an active process that remains to be defined.