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Regulation of IgE in Mice

The aim of this review is not to analyze all that has been published on IgE production and suppression in mice, as two excellent monographs were published recently covering this subject (Tada 1975, Ishizaka 1976), but to report our own recent experiments obtained mostly in the SJL strain of mice. It is an old clinical observation that parasitic infestations induce hypersensitivity reactions to the antigens of the parasite and eosinophilia. The most striking immunological property of helminth infections is a capacity to provoke high levels of IgE and IgE antibodies in their host' (Ogilvie & Jones 1973). Long before the distinction of lymphocytes into B and T cell populations, it was shown using hapten-protein conjugates that a good secondary antihapten antibody response can be obtained only if the hapten-protein conjugate is the same as that used for priming and this fact was called the carrier effect (Ovary & Benacerraf 1963). It has also been shown that a good secondary anti-hapten response can be obtained even when the animals are reinjected with a conjugate of the same hapten to a different (second) protein, provided that the animals were primed previously also with the second protein (Mitchison 1969). It is well established today that the carrier effect is due to the recognition of the carrier by the T lymphocytes and that the anti-hapten antibody is produced by B lymphocytes (Raff 1970).