One highly puzzling aspect of the phenomenon of the delayed hypersensitivity of infection, namely, the necessity for the presence of the entire organism in the tissues in order that the hypersensitive state be induced, has been dealt with in previous publications in relation to tuberculosis (1, 2). Although it is well known in the case of the tubercle bacill~s timt the protein of the organism is the antigenic component responsible for the hypersensitive state/this substance in isolated form is powerless to bring about the typical hypersensitivity which follows either infection or the injection of killed bacterial cells, and this despite the well established antigenic properties of such protein. It was demonstinted that the protein could become effective ff at the same time the animal received another component of the bacillus; i.e., the waxy lipid extractable with chloroform (3). A series of criteria established that the hypersensitive state so induced fulfills in all particulars that which follows on the heels of tuberculous infection.In work of this nature, a point of confusion may arise from the failure to distinguish--in the mind of the investigator as well as in the inductive procedures employed--the nature of delayed hypersensitivity and the basic differences segregating it from hypersensitivity of the immediate type, including anaphylaxis, Arthns reactivity, and the human "atopic" states. Briefly stated, the differences are these:1. Immediate hypersensitive reactions follow exposure to antigen within seconds or minutes. Delayed reactions require hours and progress relatively slowly.2. In immediate hypersensitivity a demonstrable humoml antibody is involved, since this will transfer the state to normal recipients. In delayed reactivity no antibody has ever been demonstrated; the only successful attempts to transfer the state have been those employing cells obtained, for example, from an induced peritoneal exuclate (4-8).

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