Leukocytes from patients with an allergy to penicillin failed to migrate when exposed in vitro to penicillin coupled to human γ-globulin. On the other hand, leukocytes from nonallergic individuals showed no inhibition of migration when exposed to the same antigen.
The sera from the allergic patients were able to sensitize leukocytes obtained from nonallergic individuals. Inhibition of migration of these sensitized leukocytes is produced upon exposure to penicillin-γ-globulin. However, a reversal of the latter inhibition of leukocyte migration was observed when the allergic sera were previously treated with penicillin G alone. The allergic sera able to sensitize leukocytes contained antibodies to penicillin. These antibodies were demonstrated by their ability to neutralize bacteriophage T4 coated with penicillin.
Some antigens show certain sensitization specificities toward tissue. Experience has demonstrated that pollen allergy is manifested mainly by respiratory signs (c.g., rhinitis, asthma). Undoubtediy the use of adjuvants almost always produces sensitization, when M. tuberculosis is used. It is difficult to establish if these findings in adjuvants are causal. If by means of this method, easily carried out in the laboratory, a delayed type of sensitization (with or without clinical findings) is acconiplishcd with antibody response, and if we know that in man 3.1. tuberculosis produces both immediate and delayed phenomena, we can reasonably assume ail immediate sensitization mechanism in man. In othclr words, an inflammatory reaction arises with certain charac-*
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