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The Journal of Immunology, Vol 155, Issue 11 5455-5462, Copyright © 1995 by American Association of Immunologists

ARTICLES

bcl-2 transgenic Lpr mice show profound enhancement of lymphadenopathy

EA Reap, NJ Felix, PA Wolthusen, BL Kotzin, PL Cohen and RA Eisenberg
Department of Medicine, University of North Carolina, Chapel Hill 07599, USA.

The lpr gene encodes a defective form of the fas gene that mediates apoptosis, and its expression results in autoantibodies and massive lymphadenopathy. bcl-2, another gene locus that affects programmed cell death, acts to inhibit apoptosis. Since multiple mechanisms controlling programmed cell death may contribute to systemic autoimmunity, the effect of the bcl-2 transgene on the lpr model was examined by crossing bcl-2 transgenic and C57BL/6-lpr mice. Compared with bcl-2-/lpr mice, bcl-2+/lpr showed dramatic increases in lymphadenopathy and T cell accumulation, but not in autoantibodies or B cell numbers. Short term transfer studies demonstrated that double negative T cells normally have a limited lifespan, and their survival is enhanced by the bcl-2 transgene. Thus, defects in separate apoptosis mechanisms may combine to produce enhanced pathologic effects.


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