Stimuli for the production and control of IgE in rats.

In Hooded Lister rats IgE responses may be induced by administration of antigen together with one of a number of adjuvants. The primary IgE response may subsequently be enhanced either specifically by a further exposure to antigen (booster response) or non-specifically by infection with helminth parasites (potentiated response). In the latter case the enhanced response is associated with a great increase in total serum IgE. The primary response itself is not significantly influenced by variations in the general theme of conventional immunization, including dose or route of administration of antigen, or the nature of the adjuvant employed. The booster response however is inhibited, a) in rats primed with a 'large' (e.g. greater than 100 microgram EA) dose of antigen and B. pertussis, and b) rats primed with any dose of antigen given in Al(OH)3 or CFA, and c) following repeated booster doses of soluble (i.e. unadjuvanted antigen even at a dosage of a few picogrammes. It is thought that each of the stimuli generate antigen specific suppressor T cells. Live worm parasites selectively, but non-specifically, stimulate heterologous antigen primed IgE responses. The evidence suggests that it may be this non-specific IgE stimulating effect rather than the parasite specific IgE response per se which leads to the great elevation of total serum IgE. Other immunoglobulin classes are not elevated in the same way. The potentiated IgE response is not susceptible to the suppressive influence generated by previous administration of large or repeated doses of the heterologous antigen. On the other hand, a parasite specific regulatory mechanism acts to prevent repotentiation of the heterologous (but not the parasite specific or total IgE) responses following reinfection. These results are discussed in relation to the work of others in rats and other species.