During the many years that tuberculin has been used in the therapy of tuberculosis, years in which it has had as enthusiastic approval as it has had unqualified condemnation by clinicians the world over, the basis of its use has centered about the idea that in some way tuberculin had value in increasing the “antibody resistance” to the infection or in desensitizing specifically against the toxic products of the infection. Just how this was induced has never been satisfactorily explained. Yet we do know definitely that if it has value in some cases, that value cannot be due to the antibody mechanism. Increase in antibody concentration in the blood need bear no relation whatever to either clinical improvement or regression.

Granted that therapeutic results may at times be observed, how are they brought about?

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