Regulation of the B cell response to T-dependent antigens by classical pathway complement.
Mice deficient in complement components C3 (C3 -/-) and C4 (C4 -/-) were found to have a profound defect in their Ab response to a T-dependent Ag (bacteriophage (phi X174). Characterization of the deficient mice demonstrated a diminished level of peanut agglutinin+ germinal centers and a failure in isotype switching despite normal B cell signaling in vitro. The nature of the defect was found to lie at the B cell level, as the T cells were primed in C3- and C4-deficient mice as well as those in wild-type mice. These results, and the finding that the defect could be partly reversed by a 10-fold increase in Ag dose, support the hypothesis that covalent attachment of complement ligands, i.e., C3b and C3d to the Ag-Ab complex, increases its immunogenicity.
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- T-Lymphocytes
- Spleen
- Mice, Mutant Strains
- Mice, Inbred C57BL
- Mice
- Male
- Lymphocyte Activation
- Immunology
- Germinal Center
- Female
Citation
Published In
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- T-Lymphocytes
- Spleen
- Mice, Mutant Strains
- Mice, Inbred C57BL
- Mice
- Male
- Lymphocyte Activation
- Immunology
- Germinal Center
- Female