Negative feedback regulation of contact sensitivity to DNFB by autoanti-idiotypic antibody

Contact sensitivity to 2,4-dinitrofluorobenzene is maximal six days after sensitization but declines rapidly, due to autoanti-idiotypic antibodies produced by the host. The studies presented here indicate that this down regulation by anti-Id is a C-independent active process involving a subset of Ia+ T cells in the immune lymph node cell population. Depleting immune LN cells of Ia+ T cells renders them insensitive to inhibition by anti-Id alone, although the same population is inhibited by treatment anti-Id plus C. This cell population is rendered sensitive to inhibition by anit-Id alone by adding untreated DNFB-sensitized LN cells but not by adding normal LN cells. Further studies showed that suppression by anti-Id-activated Ia+ T cells occurs locally at the skin test site and is antigen nonspecific. These data indicate that the natural regulation of CS to DNFB by autoanti-Id antibodies involves a negative feedback regulatory loop.