Control by Ig genes of the responsiveness to a neutralization viral B cell epitope
Leclerc, C.; Martineau, P.; Charlot, B.; Delpeyroux, F.; van der Werf, S.; Hofnung, M.
Journal of Immunology 158(7): 3252-3258
1997
ISSN/ISBN: 0022-1767 PMID: 9120281 Document Number: 477512
A study was made of the capacity of 7 strains of mice to produce antibodies against the neutralization poliovirus C3 B cell epitope, chemically or genetically linked to different carrier proteins (MaIE and keyhole limpet haemocyanin) or to recombinant hepatitis B surface antigen particles. Following immunization with the different immunogens, all strains of mice developed high antibody titres against the carrier proteins. However, only 4 strains developed a significant antibody response against the poliovirus C3 B cell epitope. In contrast to BALB/c, DBA/1, DBA/2 and 129sv mice, C57BL/6, C3H and CBA/J mice failed to produce anti-C3 antibodies after immunization with the various C3 immunogens. It was concluded that, using various H-2-congenic strains on the BALB/c or C57BL/10 background, the response to the C3 B cell epitope was not controlled by MHC genes. In contrast, analysis of anti-C3 antibody responses in IgH-congenic mouse lines on the BALB/c or C57BL/6 background demonstrated that the capacity to respond to this B cell epitope was controlled by genes closely linked to VH genes. The results therefore demonstrate that VH polymorphism can limit antibody response to a viral neutralization epitope, and therefore has important implications for vaccine development.