title: Complement receptor expression and activation of the complement cascade on B lymphocytes from patients with systemic lupus erythematosus (SLE).
abstract: It has previously been reported that the expression of the complement receptors, CR1 on erythrocytes and blood leucocytes and CR2 on B cells, is reduced in patients with SLE, and that the reduced expression of CR1 on erythrocytes is related to disease activity. We have earlier demonstrated that normal B cells are capable of activating the alternative pathway (AP) of complement in a CR2-dependent fashion. In this study we have investigated whether disturbances in this activity may be related to the altered phenotype of SLE B cells. Flow cytometry was used to measure expression of complement receptors and regulatory proteins on B cells from SLE patients, as well as the deposition of C3 fragments occurring in vivo or after in vitro AP activation. We have confirmed, for a proportion of the patients studied, reduced expression of CR1 and CR2 on B cells, and shown a consistency between low CR2 expression and reduced in vitro AP activation in the presence of homologous, normal serum. In addition, the B cells, like erythrocytes, bear raised levels of in vivo-deposited C3dg, but not C3b fragments, compared with normal B cells. The erythrocytes from SLE patients were unable to inhibit in vitro AP activation by B cells in homologous serum. Finally, we demonstrated an inverse relationship between SLE disease activity index (SLEDAI) and the expression of complement receptor 2 (CR2) on SLE B cells. Thus, determination of CR2 on B cells may emerge as an additional laboratory tool in the assessment of SLE activity.
authors.affiliation: Department of Medical Microbiology, Odense University, Denmark.
authors.forename: H V
authors.initials: HV
authors.lastname: Marquart
authors.forename: A
authors.initials: A
authors.lastname: Svendsen
authors.forename: J M
authors.initials: JM
authors.lastname: Rasmussen
authors.forename: C H
authors.initials: CH
authors.lastname: Nielsen
authors.forename: P
authors.initials: P
authors.lastname: Junker
authors.forename: S E
authors.initials: SE
authors.lastname: Svehag
authors.forename: R G
authors.initials: RG
authors.lastname: Leslie
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal / Q000276:immunology; D001402:B-Lymphocytes / Q000378:metabolism*; D003176:Complement C3 / Q000032:analysis* / Q000378:metabolism; D003179:Complement C3b; D015932:Complement C3c / Q000032:analysis / Q000378:metabolism; D015933:Complement C3d / Q000032:analysis / Q000378:metabolism; D003170:Complement Pathway, Alternative / Q000276:immunology*; D004912:Erythrocytes / Q000276:immunology / Q000378:metabolism; D005260:Female; D006801:Humans; D007962:Leukocytes / Q000737:chemistry / Q000378:metabolism; D008180:Lupus Erythematosus, Systemic / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D011951:Receptors, Complement / Q000096:biosynthesis*; D017464:Receptors, Complement 3d / Q000096:biosynthesis
chemical_list: D000911:Antibodies, Monoclonal; D003176:Complement C3; D011951:Receptors, Complement; D017464:Receptors, Complement 3d; C034772:complement C3g; D003179:Complement C3b; D015932:Complement C3c; D015933:Complement C3d