Antigen receptors on murine T lymphocytes in contact sensitivity. III. Mechanism of negative feedback regulation by auto-anti-idiotypic antibody.

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Abstract
Contact sensitivity (CS) to 2,4-dinitrofluorobenzene (DNFB) is maximal 6 d after sensitization but declines rapidly. Previous studies have shown that this rapid decline is due to auto-anti-idiotypic (anti-Id) antibodies produced by the host. The present study was done to investigate the mechanism(s) involved in his down-regulation of the effector phase of the CS reaction. Using transfer of CS to mimic the natural effector phase, we found that the inhibition of transfer by treating DNFB-sensitized lymph node (LN) cells with either auto-anti-Id or syngeneic anti-Id serum is complement (C) independent. This inhibition requires Ia+ T cells in the immune population. Depleting immune LN cells of Ia+ T cells rendered them insensitive to inhibition by anti-Id alone, although the same population is inhibited by anti-Id plus C. This cell population is rendered sensitive to inhibited by anti-Id alone by addition of untreated DNFB-sensitized LN cells, but not by addition of normal LN cells. Further studies showed that the suppression of immunity by anti-Id-activated Ia+ T cells is not systemic, but rather occurs locally at the skin test site and is antigen nonspecific. We interpret these data to indicate that the natural regulation of CS to DNFB by auto-anti-Id antibodies is an active process that involves a negative feedback regulatory loop.