SummaryCBA/N mice have an X‐linked B cell defect which prevents them from responding to non‐mitogenic thymic independent (TI‐II) antigens such as dinitrophenylated (DNP‐AGG) Ficoll. The F1male progeny of CBA/N female mice express the same defect. Spleen cell suspensions from such defective mice (CBA/N X C3H/HeN F1males) could not respond to DNP‐AGG‐Ficoll followingin vitroimmunization and subsequent transfer into irradiated, syngeneic, F1male recipients as expected. In contrast, normal CBA/N X C3H/HeN F1female spleen cells could respond and effect a ‘rescue'; they mounted strong plaque‐foriming cell 7 days afterin vitroexposure to DNP‐AGG‐Ficoll and subsequent transfer into irradiated F1male recipients. Defective F1male spleen cells could bind significant quantities of DNP‐AGG‐Ficoll, however, after,in vitroexposure. Extensive washing of these spleen cells could not reverse this binding. Such DNP‐AGG‐Ficoll‐exposed and washed F1male spleen cells could, after transfer, aid normal untreated F1female cells in their rescue function. The defective F1male spleen cells could convey immunogenic quantities of DNP‐AGG‐Ficoll to the ‘rescuing’ F1female cells.Mitomycin treatment of F1male cells did not interfere with their conveyor function. Goat anti‐mouse μ serum impeded the passive antigen conveyor function of defective F1male cells as did prior exposure to high concentrations of free DNP‐AGG hapten. Our data support the view that the B cell defect of CBA/N X C3H/HeN F1male mice does not relate to antigen binding, but rather to an inability to be effectively triggere
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