Delayed advent of stringent, non-H-2 genetic regulation of the antibody response to a protein antigen.
The role of non-H-2 gene(s) in the control of the antibody response to three lysozymes was investigated. Upon secondary challenge, A/J (H-2a) mice generated at least a 25-fold greater anti-lysozyme plaque-forming cell response than did B10.A (H-2a) mice. Nearly equal, strong peak primary responses, predominantly IgG in nature, were obtained from both A/J and B10.A mice after a single challenge with lysozyme in complete Freund's adjuvant. However, clear differences in responses are seen within 5 days after the peak primary plaque-forming response and by day 28 at the serum antibody level. B10.A mice never equal their primary responses, whereas A/J mice demonstrate positive immune memory. It appears that a non-H-2 gene(s) that regulates the overall antibody level to a protein antigen becomes manifest only after an initial antibody response.
D000818:Animals; D000917:Antibody Formation; D000941:Antigens / Q000276:immunology*; D001717:Birds; D002645:Chickens; D003433:Crosses, Genetic; D006183:H-2 Antigens / Q000235:genetics*; D006462:Hemolytic Plaque Technique; D006801:Humans; D007156:Immunologic Memory; D007525:Isoelectric Focusing; D051379:Mice; D008805:Mice, Inbred A; D009113:Muramidase / Q000276:immunology*
D000941:Antigens; D006183:H-2 Antigens; D009113:Muramidase