Sheep erythrocytes ingested by guinea pig peritoneal macrophages in vitro, and permitted to undergo digestion for various periods, were found after some hours to lose the capacity to induce antibodies while gaining the ability to invoke delayed hypersensitivity. These observations may be related to the known predilection of small molecular immunogens to act as good inducers of delayed reactivity and poor stimulators of antibody. They may be related also to the activity of mycobacterial adjuvant as a vehicle for the induction of delayed hypersensitivity on the basis that this melange activates macrophages to phagocytose and enzymatically degrade macromolecular antigens rapidly. The thesis that small fragments of antigenic molecules may preferentially invoke hypersensitivity can be interpreted on the basis of current concepts of multicellular involvements in immune responses.
In recent publications, Uhr and coworkers (1, 2) have described the induction of "delayed hypersensitivity" in guinea pigs by means of injections of antigen-antibody complexes in the region of antibody excess. The intradermal route was suggested as a determinant of the degree of sensitivity attained, although injections were made into the footpads rather than into the skin. This hypersensitivity is described as developing against the antigenic moiety of the complex. This state has been described on the basis of reactivity occurring 24 hours after skin test injections, and in the absence of humoral antibodies. No other objective criteria have been applied to its delineation. However, it appears from the descriptions given that this reactivity resembles that seen in allergy of the delayed type. Good and coworkers (2 a) have reported similar findings in normal and agammaglobulinemic patients injected with diphtheria toxoid-horse antitoxin floccules.These observations called to mind similar reactive states observed by a number o;f investigators (3-7) some years ago, in human beings and animals, following small injections of foreign sera. In those instances the "delayed" reactive state proved to be evanescent, coming on usually within several days after the initial sensitizing injections, and at various times disappearing to be succeeded by humoral antibodies and the more conventional wheal and flare or the Arthus type of skin reactivity. It seemed to us that the "delayed" responses reported by Uhr et al. might be further examples of these observations rather than of the more stable, persisting, delayed reactivity seen to occur during infectious processes, or following the injection of antigens along with killed tubercle bacilli (22) or a certain lipoidal component of these into normal animals (8-12), or after exposure of the skin to inducers of contact dermatitis. The experiments to be described have demonstrated that the hypersensitivity of apparently delayed type, which occurs after injections of antigen-antibody complexes, follows equally well after injections of antigen alone, as the older *
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