Generation of agammaglobulinaemic mice by prenatal and postnatal exposure to polyclonal or monoclonal anti-IgM antibodies.

Improved experimental conditions are described for the treatment of mice with anti-IgM antibody, which subsequently lead to B-cell deficiency and agammaglobulinaemia. Antibody transmitted via maternal milk alone was found to be more efficient in inducing suppression of serum immunoglobulin isotypes than prenatal transmission or postnatal intraperitoneal injections alone. However, the combined treatment by all three routes of exposure to anti-IgM resulted in total B-cell suppression associated with undetectable levels of all serum immunoglobulin isotypes. Furthermore, suppression of B-cell generation was also achieved with a rat monoclonal mu-specific antibody. The possibility of generating agammaglobulinaemic mice may be useful for investigating the influence of B cells on the generation of T-cell reactivities, and for analysing the effects of monoclonal antibodies in the absence of interfering serum immunoglobulin.