Functional Antigen Binding by the Defective B Cells of CBA/N Mice

Summary

CBA/N mice have an X-linked B cell defect which prevents them from responding to nonmitogenic thymic independent (TI-2) antigens such as dinitrophenylated DNP-Ficoll (1,2). The F₁ male progeny of CBA/N female mice express the same defect. Spleen cell suspensions from such defective mice (CBA/N X C3H/HeN F₁ males) could not repsond to DNP-Ficoll following in vitro immunization and subsequent transfer into irradiated, syngeneic, F₁ male recipients as expected. In contrast, normal CBA/N X C3H/HeN F₁ female spleen cells could respond and effect a “rescue”; they mounted strong plaque-forming cell responses 7 days after in vitro exposure to DNP-Ficoll and subsequent transfer into irradiated F₁ male recipients. Defective F₁ male spleen cells, however, could bind significant quantities of ¹²⁵I-DNP-Ficoll after in vitro exposure. Extensive washing of these spleen cells could not reverse this binding. Such DNP-Ficoll-exposed and washed F₁ male spleen cells could, after transfer, aid normal untreated F₁ female cells in their rescue function. The defective F₁ male spleen cells could convey immunogenic quantities of DNP-Ficoll to the “rescuing” F₁ female cells.

Mitomycin treatment of F₁ male cells did not interfere with their conveyor funciton. Goat anti-mouse µ serum impeded the passive antigen conveyor function of defective F₁ male cells as did prior exposure to high concentrations of free DNP hapten. Our data support the view that the B cell defect if CBA/N X C3H/HeN F₁ male mice does not relate to antigen binding, but rather to an inability to be effetively triggered by certain cell-bound polymeric antigens.