title: 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.
authors.affiliation: Medizinische Universitätsklinik B, Kantonsspital Basel, Switzerland.
authors.forename: E
authors.initials: E
authors.lastname: Lach-Trifilieff
authors.forename: J
authors.initials: J
authors.lastname: Marfurt
authors.forename: S
authors.initials: S
authors.lastname: Schwarz
authors.forename: S
authors.initials: S
authors.lastname: Sadallah
authors.forename: J A
authors.initials: JA
authors.lastname: Schifferli
mesh_terms: D000373:Agglutinins / Q000097:blood; D000375:Aging / Q000097:blood / Q000276:immunology; D000744:Anemia, Hemolytic, Autoimmune / Q000097:blood / Q000276:immunology; D003450:Cryoglobulins; D004797:Enzyme-Linked Immunosorbent Assay; D004912:Erythrocytes / Q000378:metabolism; D015658:HIV Infections / Q000097:blood / Q000276:immunology*; D006801:Humans; D015151:Immunoblotting; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000276:immunology*; D017463:Receptors, Complement 3b / Q000096:biosynthesis* / Q000097:blood / Q000502:physiology; D012156:Reticulocytes / Q000276:immunology / Q000378:metabolism* / Q000502:physiology
chemical_list: D000373:Agglutinins; D003450:Cryoglobulins; D017463:Receptors, Complement 3b; C029443:cold agglutinins