Regulation of the B cell response to T-dependent antigens by classical pathway complement.

摘要: Mice deficient in complement components C3 (C3 -/-) and C4 (C4 were found to have a profound defect their Ab response T-dependent Ag (bacteriophage (phi X174). Characterization of the mice demonstrated diminished level peanut agglutinin+ germinal centers failure isotype switching despite normal B cell signaling vitro. The nature was lie at level, as T cells primed C3- C4-deficient well those wild-type mice. These results, finding that could be partly reversed by 10-fold increase dose, support hypothesis covalent attachment ligands, i.e., C3b C3d Ag-Ab complex, increases its immunogenicity.