Journal of Experimental Medicine, Vol 155, 820-830, Copyright © 1982 by Rockefeller University Press
Antigen receptors on murine T lymphocytes in contact sensitivity. III. Mechanism of negative feedback regulation by auto-anti-idiotypic antibody
JW Moorhead
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.
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