The changes in a wide variety of in vivo and in vitro tests following a long course of low antigen dosage hyposensitization therapy in fifteen asthmatic patients with house dust mite allergy are reported.
Evidence of clinical improvement was shown by decreased bronchodilator requirement. Bronchial challenge testing showed a significant increase in bronchial tolerance to mite antigen. Nasal and skin tests with mite extract, however, did not show a significant change.
In contrast to the development of bronchial tolerance and to the clinical improvement, some of the in vitro tests seemed to provide evidence of hypersensitization. The leucocyte test, for example, showed increased sensitization to the mite antigen, as well as an increase in histamine release by anti-IgE serum. Total serum IgE was also increased, but this was apparently due to non-allergen specific IgE.
Although the leucocyte test showed increased sensitization to mite antigen, serum reaginic activity as measured by the passive sensitization of human lung did not show any increase. Thus, there seemed to be a difference in the affinity of allergen-specific IgE for leucocytes as compared with lung tissue. It also appeared that leucocyte response to antigen bore no relationship to sensitization of other tissues, particularly the bronchial tree.
The mechanism of clinical hyposensitization by low dosage immunotherapy is discussed. It is suggested that apart from the development of blocking antibodies, other mechanisms seem likely. Among these are a change in the affinity of IgE antibodies for different tissues, and a competition between non-specific IgE (produced in excess as a result of immunotherapy) and allergen-specific IgE.