CBA/N mice have an X-linked B-cell defect. It prevents them from mounting active immune responses to soluble, nonmitogenic, polysaccharide antigens. The F1 male progeny of defective CBA/N female mice also harbor the same defect. Lymphoid cell suspensions prepared from these defective mice and appropriate controls were examined for their capacity to bind 125I-labeled, dinitrophenylated Ficoll, a representative polysaccharide antigen. In general, lymphoid cells bound substantially greater quantities of this antigen than nonlymphoid cells; however, lymphoid cells from defective F1 male mice differed little, if at all, from the lymphoid cells of normal F1 female mice. Direct binding of this radiolabeled antigen by spleen cell suspensions was minimally affected by depletion of functional T cells or by depletion of glass wool-adherent cells. Lymphoid cells consistently bound only a small fraction of the available radiolabeled antigen at all concentrations tested and progressive differences in direct binding by normal and defective spleen cells were not discernable. In addition, immune spleen cells differed only slightly from unprimed spleen cells in their capacity for direct antigen binding. The data are interpreted to indicate the presence of a high-capacity system for nonspecific association of this radiolabeled Ficoll antigen with lymphoid cell surfaces. The high-capacity system for nonspecific association between antigen and lymphoid cells serves to obscure immunologically significant binding between radiolabeled Ficoll antigens and normal and defective lymphoid cells. In all probability, the failure of lymphoid cells from CBA/N and F1 male mice to respond to dinitrophenylated Ficoll cannot simply be attributed to any intrinsic failure to bind this antigen.

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