Severe combined immune-defective (SCID) mice reconstituted with immunoglobulin heavy chain-disparate spleen (SP) and peritoneal cavity (PerC) B cells exhibit serologic dominance of IgM bearing the PerC allotype. Immunization fails to elicit IgM production from donor SP B cells although flow cytometric analyses indicate the presence of these cells in the spleen of (SP + PerC)-->SCID chimeras. This observation suggests that donor SP B cell function is absent or inhibited in the SCID chimera. In this report, ELISAspot and proliferation assays were employed to further investigate the functional properties of B cells in these mice. Plasma cells derived from the donor SP were present in the spleen of SCID recipients at a lower number than those derived from donor PerC B cells. Spleen cells isolated from SCID recipients could be activated with insolubilized MAbs directed against IgM or IgD allotypes expressed by either the SP or PerC B cell donor. In contrast, the peritoneal cavity of SCID chimeras lacked B cells responsive to MAbs specific for the donor SP IgM and IgD allotypes. These results demonstrate that B cells derived from the SP donor are functional in (SP + PerC)-->SCID chimeras.
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