Recall of Specific Suppression: Co-Dominance of Suppression after Primary or Secondary Antigen Stimulation

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Abstract
Mouse spleen cells primed in vivo with β-galactosidase (GZ), and cultured in vitro with trinitrophenyl β-galactosidase (TNP-GZ), make a very poor anti-TNP response compared to cultures of normal spleen cells. The lack of response is caused by active suppression as indicated by cell mixture experiments. At 2-months following priming, while the helper effect predominates, suppression can be recalled by rechallenge of the mice with GZ. Both primary suppression (after a single injection) and secondary suppression (after two injections) reduce the response of normal or carrier-primed helper cells at equivalent cell ratios in mixture experiments. Both kinds of suppression are carrier specific, selectively suppress high avidity antibody production, and require cell division to suppress the response of normal cells. The only difference between primary and secondary suppression is that primary suppression is obliterated in cultures which are not challenged with antigen until 24 hr after cultures are established. Secondary suppression is still observed when cultures receive TNP-GZ at 24 hr. Suppression appears to be an early component of both primary and secondary responses. The regulatory function of such suppression may be the delay of antibody secretion.