Regulation of murine IgE production: importance of a not-yet-described T cell for IgE secretion demonstrated in SJA9 mice.

To investigate why SJA9 mice do not produce IgE antibody, we took advantage of the adoptive transfer method and the carrier effect. Antibody-producing B cells (donor I) were primed with 2,4-dinitrophenylated ovalbumin (DNP-OVA) and carrier-specific T cells (donor II) were primed with keyhole limpet hemocyanin (KLH). The recipients were challenged with DNP-KLH. When 0.2 micrograms of DNP-OVA was used and the donor II cells were from SJL mice the recipient produced anti-DNP IgE. When donor I cells were from the SJL strain and donor II cells were from the SJA9 strain the recipient produced anti-DNP IgE. This pointed to a T-cell defect (absent or functionally inactive T epsilon o cell) in the SJA9 strain, which could be corrected either by injecting unprimed T cells from the SJL strain into the SJA9 donor I or by infection with Nippostrongylus brasiliensis, a hookworm, after priming. It seems that in the SJA9 strain in the absence of functioning T epsilon o cells isotype-specific (IgE) suppression, described previously in the SJL strain, is more pronounced, because when the SJA9 donor I was primed with 1 microgram of DNP-OVA only trace amounts of anti-DNP IgE were produced with SJL donor II cells.