Complement Receptor 1 (CD35) on Human Reticulocytes: Normal Expression in Systemic Lupus Erythematosus and HIV-Infected Patients

Abstract

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 CR1 on the red cell lineage. Therefore, we analyzed the expression of CR1 on reticulocytes (R) vs erythrocytes (E). Healthy subjects had a significant higher CR1 number per cell on R (919 ± 99 CR1/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 FACS analysis, which showed that all R expressed CR1, whereas a large fraction of 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 intravascular loss was best exemplified in a patient with factor I deficiency whose CR1 dropped from 520 CR1/R to 28 CR1/E, i.e., 18.6-fold loss. In one SLE patient and in the factor I-deficient patient, the FACS data were consistent with a loss of CR1 already on some R. In conclusion, CR1 is lost progressively 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.

Changes of Red Blood Cell Surface Markers in a Blood Doping Model of Neocytolysis

“…Specifically assayed were adhesion molecules (CD36 [thrombospondin receptor], CD44, CD49d [very late antigen 4], CD242 [intercellular adhesion molecule 4], and phosphatidyl serine); additional antigens reported to mark young cells (CD35 [complement receptor 1], CD55 [decay-accelerating factor], CD71, and CD324 [E-cadherin]); and markers of older RBC (CD235a [glycophorin A] and hemoglobin A). 13-18 From this screened panel, CD35, CD44, CD55, and CD71 seemed differentially expressed and were further studied.…”

Gene expression analysis revealed downregulation of complement receptor 1 in clonal B cells in cold agglutinin disease

“…Downregulation of CR1 (CD35) expression on erythrocytes has previously been reported in other diseases, including autoimmune disease [ 26–29 ]. Reduced expression of CR1 (CD35) on erythrocytes in CAD has previously been shown in case series, but systematic studies are lacking [ 26 , 30 , 31 ].…”