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Developmental analyses of B cell differentiation are consistent with the existence of at least two distinct lineages . Thus, adult bone marrow solely regenerates the commonest (Ly-1 -) lineage, while Ly-1 + B cells reconstitute the Ly-1 + B cell lineage (1). CBA/N mice carrying the X-linked immunodeficiency gene (xid)
show a defective differentiation of B lymphocytes (2) . They lack all Ly-1 + B cells as well as the normally predominant subpopulation within the Ly-1 - lineage (3) .
Functional studies (4) indicated that Ly-1 + B cells are responsible for the production
of most of the autoantibodies, while those B cells in the Ly-1 - lineage
participate in the conventional responses to "foreign" antigens. These observations
may account for both the protection conferred against autoimmune disease,
when the xid genetic defect is bred into lupus-prone strains, and the CBA/N
mice unresponsiveness to many bacterial antigens (5, 6) .
Administration of the immunosuppressant cyclosporine A (CsA) at the time of
autologous bone marrow reconstitution results in systemic autoimmunity in
CBA/N mice. Besides, these mice show a severe diminution, if not absence, of
bone marrow pre-B cells, but increased amounts of activated B cells and autoantibodies (7). We have now studied the possibility that Ly-1 + B cell precursors
may exist in CBA/N mice and report here experiments indicating that this is indeed the case
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