Abstract
Abstract The duration of maximal contact sensitivity in the mouse is regulated, at least in part, by specific antibodies. Mice sensitized with optimal doses of 2,4-dinitrofluorobenzene (DNFB) develop maximum delayed hypersensitivity in 4 to 5 days as measured in vivo by ear swelling. The intensity of this reaction declines rapidly, and by 12 days post-sensitization significant immunity is no longer detectable. Serum taken from animals 9 to 15 days post-sensitization will block the ability of DNFB-immune lymph node (LN) cells to passively transfer immunity. The suppressive molecules are immunoglobulins, but they do not have anti-DNP activity and are not associated with DNP as antigen-antibody complexes. The suppressive serum is antigen specific, i.e., it blocks DNFB-immune LN cells but not TNCB- or oxazolone-immune LN cells, and it lacks strain specificity in inhibiting passive transfer. The suppressive serum can be adsorbed by DNFB-immune LN cells (both syngeneic and allogeneic), but not by normal LN cells. Furthermore, the suppressive activity of the serum is adsorbed by and can be recovered from an affinity column conjugated with purified mouse anti-DNP antibodies. We conclude that blocking antibodies arise during sensitization with DNFB and down-regulate the duration of sensitivity. These antibodies are directed against surface components of immune LN cells. They possess anti-idiotype activity and represent part of the immunoregulatory elements within a complex network of anti-idiotype/idiotype interaction.
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