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The Journal of Immunology, Vol 147, Issue 8 2536-2539, Copyright © 1991 by American Association of Immunologists
ARTICLES |
D Nemazee, C Guiet, K Buerki and A Marshak-Rothstein
Basel Institute for Immunology, Switzerland.
Data are presented showing that MRL/lpr in equilibrium DBA/2 tetraparental (allophenic) chimeras, unlike conventional lpr/lpr---- +/lpr bone marrow chimeras, fail to develop graft-vs-host disease; instead they develop full-blown lymphoproliferation and autoantibody formation typical of unmanipulated MRL/lpr mice. The increase in the splenic and especially the lymph node mass is comprised predominantly of MRL/lpr-derived cells and all of the serum IgG2a is MRL/lpr derived. This dominance of MRL/lpr lymphoid activity occurred even in chimeras where greater than 90% of the skin and/or bone marrow cells were of the DBA/2 type. These results demonstrate the failure of the lpr environment to recruit normal B and T cells into the autoimmune process, the inability of normal cells to suppress MRL/lpr disease, and indicate further that the lpr mutation has an intrinsic effect on lymphocytes of both the B and T lineages.
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