title: Decreased levels of complement receptor 1 (CD35) on B lymphocytes in persons with HIV infection.
abstract: Previous studies have shown that complement receptor 1 (CR1) expression on erythrocytes is decreased under several conditions including HIV infection and autoimmune diseases. The goal of this study was to determine whether expression of CR1 on peripheral blood B cells, where this receptor plays a role during immune responses, is altered in persons with HIV infection. The B cells from rheumatoid arthritis (RA) patients were also assessed since this represents a group with known complement and B cell abnormalities. The CD19+ B cells from persons with either HIV infection or RA had significantly reduced levels of CR1 when compared with control donors (75 and 72% CR1+ versus 94% CR1+ for control donors). The reduction of B cell CR1 occurred in both the percentage of B cells positive for CR1 and the levels of CR1 found on positive cells. In contrast, CR1 on monocytes was not reduced. As shown in previous studies, CR2 was also found to be reduced on B cells from the HIV-infected persons and there was extensive overlap between the B cell subsets which lacked expression of CR1 and CR2. The complement receptor-negative B cells found in HIV-infected persons were not immature or activated as defined by their lack of expression of CD10 or B7, respectively. Elevated levels of C4d, a classical complement pathway-activation product, were detected in plasma from both HIV-infected and RA patients. These studies suggest that chronic complement activation occurring in persons with HIV infection or RA can affect the complement receptor phenotype of peripheral blood B cells. Since complement receptors are involved in activation of B cells, the subset that lacks CR1 may represent cells that have encountered immune complexes and may therefore be stimulated. Additionally, the downregulation of complement receptors may have significant effects on the ability of B cells to capture and present opsonized antigens.
authors.affiliation: Department of Immunology/Microbiology, Rush Medical School, Chicago, Illinois 60612.
authors.forename: L G
authors.initials: LG
authors.lastname: Munson
authors.forename: M E
authors.initials: ME
authors.lastname: Scott
authors.forename: A L
authors.initials: AL
authors.lastname: Landay
authors.forename: G T
authors.initials: GT
authors.lastname: Spear
mesh_terms: D000936:Antigen-Antibody Complex / Q000276:immunology / Q000378:metabolism; D015703:Antigens, CD / Q000032:analysis; D018941:Antigens, CD19; D000944:Antigens, Differentiation, B-Lymphocyte / Q000032:analysis; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000473:pathology; D001402:B-Lymphocytes / Q000737:chemistry* / Q000276:immunology / Q000648:ultrastructure; D003167:Complement Activation; D003181:Complement C4 / Q000032:analysis; D015935:Complement C4b; D003171:Complement Pathway, Classical; D005434:Flow Cytometry; D005453:Fluorescence; D015658:HIV Infections / Q000097:blood* / Q000473:pathology; D006801:Humans; D010446:Peptide Fragments / Q000032:analysis; D017463:Receptors, Complement 3b / Q000032:analysis*; D017464:Receptors, Complement 3d / Q000032:analysis
chemical_list: D000936:Antigen-Antibody Complex; D015703:Antigens, CD; D018941:Antigens, CD19; D000944:Antigens, Differentiation, B-Lymphocyte; D003181:Complement C4; D010446:Peptide Fragments; D017463:Receptors, Complement 3b; D017464:Receptors, Complement 3d; D015935:Complement C4b; C032261:complement C4d