An extensively modified protein antigen (methylated bacterial α-amylase, M-BαA) which was neither reactive with anti-BaA antibody nor able to induce a humoral anti-BαA response, retained the ability to prime native BαA-specific T cells which were responsible for the enhanced anti-BαA response to subsequent immunization with BαA and delayed hypersensitivity (DH). The splenic T cell-rich fraction from mice primed with M-BαA collaborated with a native BαA-primed B cell-rich fraction to give a good adoptive IgG anti-BαA response in syngeneic irradiated mice, whereas M-BαA-primed B cell fractions failed to cooperate with native BαA-primed T cell fractions. Splenic T cells from mice given a subcutaneous (s.c.) injection of M-BαA in complete Freund's adjuvant (CFA) exhibited DH in syngeneic cyclophosphamide-treated mice. In the present study, native and methylated BαA were tested for their ability to generate suppressor T cells capable of inhibiting the development of DH.
An intraperitoneal (i.p.) injection of either native or methylated BαA in incomplete Freund's adjuvant (IFA) interferred with the development of DH to M-BαA by an s.c. injection of the same antigen in CFA. Transfer of spleen cells from mice given an i.p. injection of either of these antigens 5 days previously, suppressed antigen-specifically induction and expression of DH in the syngeneic recipient mice. The suppressive activity was sensitive to treatment with anti-θ antiserum plus complement. These results indicate that the early phase of inhibition of DH after an i.p. injection is in part mediated by suppressor T cells and that M-BαA cross-reacts with native BαA at the suppressor T cell level as well as the level of effector T cells in DH.