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The immunogenic capacity of protein antigens has been compared for the free and peritoneal exudate cell (PEC)-bound forms. The response of OBA mice to BSA provides the reference system, but lysozyme, ovalbumin, HSA and modified BSA were also studied. Uptake is approximately equally efficient in vivo and in vitro. PEG-bound antigen, estimated by radioactivity is far more potent than the free form in inducing primary immunization. The following properties were also found: (i) viable PEG are required; (ii) irradiation of the cell donor 2–7 days before giving antigen inhibits immunization, but irradiation after uptake does not do so; (iii) mice are susceptible to immunization during their phase of recovery from paralysis; (iv) PEG do not retain large amounts of antigen for long; (v) the activity does not depend solely on a minor, phagocytosis- prone fraction of the antigen; (vi) allogeneic transfer of PEG reduces their immunogenic capacity; (vii) paralysed hosts are not susceptible to immunization, but PEG from paralysed donors are effective; and (viii) the enhancement of immunogenic capacity does not apply to the secondary response. The conclusion may be drawn that the retention of small quantities of antigen by macrophages plays an essential role in some, but probably not all types of immune response.

Immunization of HSA-tolerant animals with sulphanil-HSA induces the formation of antibodies that react with native HSA. To test whether the anti-HSA response does actually represent complete restoration of the original reactivity, the antibodies produced following immunization of tolerant animals with sulphanil-HSAS were compared to those produced by normal rabbits immunized with the native antigen. Gel-diffusion analysis of the precipitins disclosed that the patterns of the two types of antibody were not completely identical. The antibodies of the 'restored' tolerant rabbits were directed mainly towards an antigenic determinant of the native HSA, to which normal rabbits immunized with HSA did not respond. When the 'restored' rabbits were challenged with native HSA after a prolonged rest period, the antibodies formed thereafter were completely identical with anti-HSA produced by normal HSA-immunized rabbits. Thus, complete restoration of the original immunological reactivity to HSA was achieved following an intermediary stage of atypical anti-HSA elicited by the conjugated protein. Attempts to break down natural tolerance to RSA by treatment with sulphanil-RSA failed to give any evidence of an autoimmune elimination of RSA. To test whether this inability to break tolerance to RSA was due to the presence of an excess of native protein, animals that had been made tolerant to HSA were immunized with a mixture of sulphanil-HSA and native HSA. Under such conditions, the termination of acquired tolerance was inhibited. The possible relevance of these observations to the cellular basis of immunological tolerance is discussed. [ABSTRACT FROM AUTHOR]