bcl-2 transgenic Lpr mice show profound enhancement of lymphadenopathy - PubMed (original) (raw)
. 1995 Dec 1;155(11):5455-62.
Affiliations
- PMID: 7594564
bcl-2 transgenic Lpr mice show profound enhancement of lymphadenopathy
E A Reap et al. J Immunol. 1995.
Abstract
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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