Please use this identifier to cite or link to this item:
http://dspace.mediu.edu.my:8181/xmlui/handle/10261/3678| Title: | Development of Ly-1+ B Cells in immunodeficient CBA/N mice |
| Publisher: | Rockefeller University Press |
| Description: | El copyright pertenece a The Rockefeller University Press 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 Peer reviewed |
| URI: | http://dspace.mediu.edu.my:8181/xmlui/handle/10261/3678 |
| Other Identifiers: | The Journal of Experimental Medicine, Vol. 166, Septembre (1987), pp. 804-809 0022-1007 http://hdl.handle.net/10261/3678 |
| Appears in Collections: | Digital Csic |
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.