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KMID : 0357119920140020247
Korean Journal of Immunology
1992 Volume.14 No. 2 p.247 ~ p.260
Effects of Monoclonal Anti-IL-4 Antibody(11B11) and Interferons on IgE Production In Vivo and Hypersensitivity Reactions I. Induction of Systemic Anaphylaxis in Mice by Antigen-specific IgG and IgG Subclasses Monoclonal Antibodies
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Abstract
The previous results showing that anti-IL-4 mAb(11B11) failed to prevent the chicken-gamma globulin(CGG0-induced active systemic anaphylaxis(ASA) in BALB/c imice in spite of a significant suppression of CGG-specific IgE response prompted us to
investigate the role of IgG Abs in the induction of ASA. The author prepared both CGG-specific polyclonal and monoclonal(IgE, IgG1, IgG2a, IgG2b and IgG3) Abs and examined their capcities to induce ASA. Mice(BALB/c) were injected i.v. with
polyclonal or
monoclonal Ab alone and were challenged i.v. with CGG 60 min after IgG injection or 24 h after IgE injection. Polyclonal Ab induced a severe anaphylactic reaction and heat treatment (56¡É, 2 h) of the Ab potentiated its ASA-inducing capacity
strongly
suggested that IgG are involved in the induction of ASA. All mice received each subclass monoclonal IgG showed anaphylactic signs;igG1 induced a moderate reaction, whereas other IgG induced a week reaction. However, injection of all subelases of
IgG
together induced a very severe reaction;about 50% of mice died. IgE alone also induced ASA, but the reaction was no stronger compared with that of IgG1. There was no corelation between ASA-inducing capacity and in vitro histamine-releasing
capacity
of
the Abs. Taken together these data provide a definite direct evidence that IgG Abs have an ability to induce ASA.
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