Suppressor Cell Pathways in Cutaneous Sensitivity

We have previously demonstrated that suppressor cells can abrogate 4-hydroxy-3nitrophenyl acetyl (NP)l-specific delayed-type hypersensitivity (DTH) responses (13). We now examine the ability of the same population of suppressor cells to abrogate cutaneous sensitivity (CS) responses. Previous studies have noted several differences between the effector T cell populations which mediate DTH and CS (4-6). In particular, DTH responses can be transferred between strains of mice sharing only the H-2I region of the murine major histocompatibility complex, in contrast to CS responses, where homology at either H-2K, I, or D is sufficient for adoptive transfer of reactivity (4, 5). Further, it has been demonstrated that T cells mediating H-2Irestricted and H-2D-restricted immune responses may bear different idiotypic receptors (6, 7). Recognizing the importance of idiotypic-anti-idiotypic interactions in the generation of antigen-specific immune suppression (3, 8), we now extend the comparison of DTH and CS responses by analyzing the mechanisms of suppression of CS reactions. Earlier investigations have implicated the involvement of two distinct T cells from the NP-tolerized lymphocyte population in the regulation of DTH immunity (1-3): induction-phase suppressor T cells (Ts ~ or Tsx), which can be generated by antigen alone; and effector-phase suppressors (Ts e or Ts2), which depend for their generation on both antigen and Ts i or idiotype-positive factor derived from Ts i. Recent evidence in another system (9) has further suggested the requirement of a third auxiliary T cell from the immune lymphocyte population for the suppression of 2,4-dinitro-1-fluorobenzene (DNFB) contact sensitivity by Ts e. The current study unifies and extends these findings, demonstrating in a single system the development of all three suppressor cell types after in vivo antigen administration.