CBA/N mice harbor an X-linked B cell defect which is transmitted by CBA/N female mice to their hybrid male progeny. Hapten-specific plaque-forming cell (PFC) responses to haptenated proteins by B cell-defective CBA/N mice and CBA/N × C3H/HeN F1 male mice can be blockaded by concomitant exposure to polysaccharide agents bearing the same hapten. Various experimental approaches were explored in an attempt to study this phenomenon in a syngeneic cell transfer system. Unprimed donor spleen cells were unable to mount adequate PFC responses to dinitrophenylated-hemocyanin (DNP-KLH) in irradiated, syngeneic recipients. DNP-KLH-primed donor spleen cells produced strong PFC responses after challenge in irradiated recipients, and these secondary responses were subject to hapten-specific blockade by DNP-derivatized polysaccharide agents. Both direct and indirect PFC responses could be blocked. DNP conjugated to bovine serum albumin also produced hapten-specific blockade in this cell transfer system. Under some cell transfer conditions normal CBA/N × C3H/HeN F1 female spleen cells were just as susceptible to hapten-specific blockade as defective F1 male spleen cells.

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