Abstract
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.
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Selected References
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