Hapten‐specific tolerance in mice. II. Adoptive transfer studies and evidence for unresponsiveness in the B cells

The suppression fo the anti‐NIP ((4‐hydroxy‐5‐iodo‐3‐nitrophenyl)acetyl) plaque‐forming cell (PFC) response elicited in mice by treatment with NIP‐coated syngeneic erythrocytes could be transferred by spleen cells into irradiated recipients. This was evidenced by the lack of an indirect anti‐NIP PFC response 7 days after cell transfer and challenge with NIP. FGG (fowl IgG). This state of specific unresponsiveness could be serially transferred by spleen cells into a second irradiated recipient. The hapten‐specific suppression in the first recipient could be reversed by addition of normal spleen cells, but not by cortisone‐resistant thymus cells. The lesion appears to be in the T cell‐depleted population, since the suppression could be reversed by supplementing with T cell‐depleted normal spleen cells. In vitro incubation of spleen cells from tolerant animals did not restore the capacity of these cells to produce an anti‐NIP PFC response in irradiated recipients. In vitro incubation of normal spleen cells with sera from tolerant animals did not prevent these spleen cells from producing a normal anti‐NIP PFC response in irradiated recipients. The adoptive secondary response response to NIP. FGG was inhibited by injection of NIP‐coated syngeneic erythrocytes on the same day as the adoptive transfer of the NIP. FGG primed spleen cells and the challenging antigen. It would seem that NIP‐coupled syngeneic erythrocytes, which are presumably poor stimulators of T cells, can suppress NIP‐specific B cells, perhaps by gaining direct access to the surface of these cells.