title: Complement opsonization is required for presentation of immune complexes by resting peripheral blood B cells.
abstract: Complement receptor 2 (CD21, CR2) is a B cell receptor for complement degradation products bound to Ag or immune complexes. The role of CD21 in mediating Ag presentation of soluble immune complexes by resting B cells was studied. Complement-coated immune complexes were formed by the incubation of influenza virus with serum from immune donors. These complexes bound to peripheral blood B cells in a complement-dependent manner. The binding required CD21 or, to a lesser extent, complement receptor 1 (CR1, CD35). B cells pulsed with immune complexes containing complement elicited a response from a panel of influenza-specific T cell clones, while those pulsed with immune complexes formed in the absence of complement did not. The expression of the early activation marker CD69 and the costimulatory molecule CD86 were not induced by CD21 ligation alone, suggesting that CD21-mediated Ag presentation occurs independently of B cell activation. Up-regulation of these markers required exposure to T cell factors elicited by the recognition of Ag derived from complement-containing immune complexes. These findings suggest that binding of Ag to CD21 enables Ag-nonspecific B cells to participate in the activation of Ag-specific T cells in a process that occurs independently of well-characterized B cell activation events.
authors.affiliation: Department of Medicine, University of Colorado Health Sciences Center, Denver 80262, USA.
authors.forename: S A
authors.initials: SA
authors.lastname: Boackle
authors.forename: M A
authors.initials: MA
authors.lastname: Morris
authors.forename: V M
authors.initials: VM
authors.lastname: Holers
authors.forename: D R
authors.initials: DR
authors.lastname: Karp
mesh_terms: D017951:Antigen Presentation; D000936:Antigen-Antibody Complex / Q000276:immunology*; D015703:Antigens, CD / Q000096:biosynthesis / Q000276:immunology; D000945:Antigens, Differentiation, T-Lymphocyte / Q000096:biosynthesis / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology*; D051940:B7-2 Antigen; D003165:Complement System Proteins / Q000276:immunology*; D019267:Hemagglutinin Glycoproteins, Influenza Virus / Q000276:immunology; D006801:Humans; D007156:Immunologic Memory; D009980:Influenza A virus / Q000276:immunology; D007376:Interleukin-2 / Q000378:metabolism; D037181:Lectins, C-Type; D008213:Lymphocyte Activation; D008211:Lymphocyte Cooperation; D008562:Membrane Glycoproteins / Q000096:biosynthesis / Q000276:immunology; D009895:Opsonin Proteins / Q000276:immunology*; D017463:Receptors, Complement 3b / Q000276:immunology; D017464:Receptors, Complement 3d / Q000276:immunology*; D015398:Signal Transduction; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology / Q000378:metabolism; D000099192:CD69 Antigens
chemical_list: D000936:Antigen-Antibody Complex; D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D051940:B7-2 Antigen; D003165:Complement System Proteins; D019267:Hemagglutinin Glycoproteins, Influenza Virus; D007376:Interleukin-2; D037181:Lectins, C-Type; D008562:Membrane Glycoproteins; D009895:Opsonin Proteins; D017463:Receptors, Complement 3b; D017464:Receptors, Complement 3d; D000099192:CD69 Antigens; C497964:CD86 protein, human