Antigen-independent suppression of the IgE immune response to bee venom phospholipase A2 by maternally derived monoclonal IgG antibodies.
The IgE immune response to ovalbumin in rats can be suppressed by prior immunization of the dams. The results reported in this paper extend this observation to include a different antigen and another species, namely the IgE immune response to bee venom phospholipase A2 (PLA2) in CBA/J mice. The degree of suppression seemed to depend on the amount of IgG antibodies transferred to the offspring. Moreover, we found that the maternally mediated suppression of the IgE response could be achieved in a completely antigen-free system in which exogenous monoclonal anti-PLA2 IgG antibodies were transferred from the dams to the offspring. The following results were obtained: (i) The IgE suppression by monoclonal IgG antibodies was induced as efficiently with one single anti-PLA2 IgG1 antibody as with a mixture of ten antibodies (nine IgG1, one IgG2b). (ii) Even after several immunizations up to an age of 6 months with a dose of PLA2 that normally induces IgE production, none of the F1 mice developed an IgE response. (iii) This long-lasting suppression was observed in mice which were first immunized at an age of 4 weeks (i.e. when low amounts of maternally derived monoclonal IgG were still present), as well as in mice which were first immunized at an age of 8 weeks, when no such maternal antibodies could be detected in their sera. The corresponding IgG responses showed, compared to normal mice, a transient enhancement in the maternally influenced mice. It is concluded that the immunological experience of the mother is of particular importance for the isotype regulation in the newborns, especially with respect to the ability to elicit an IgE response. The possible implications for the development of allergic diseases in humans are discussed.
Biochemisches Institut, Medizinische Fakultät, Christian-Albrechts-Universität, Kiel, Germany.
M
M
Seeger
H J
HJ
Thierse
H
H
Lange
L
L
Shaw
H
H
Hansen
H
H
Lemke
D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology*; D001514:Bee Venoms / Q000276:immunology*; D005260:Female; D007108:Immune Tolerance; D007112:Immunity, Maternally-Acquired; D007114:Immunization; D007073:Immunoglobulin E / Q000096:biosynthesis*; D007074:Immunoglobulin G / Q000276:immunology*; D051379:Mice; D008808:Mice, Inbred CBA; D010741:Phospholipases A / Q000276:immunology*; D054467:Phospholipases A2; D011247:Pregnancy
D000911:Antibodies, Monoclonal; D001514:Bee Venoms; D007074:Immunoglobulin G; D007073:Immunoglobulin E; D010741:Phospholipases A; D054467:Phospholipases A2