THE BCL-2 PROTOONCOGENE IS OVEREXPRESSED IN SYSTEMIC LUPUS-ERYTHEMATOSUS

Systemic Lupus Erythematosus (SLE) is a disease in which lymphoid hype r-reactivity occurs. Whether this is primary or secondary is not alway s clear. SLE occurs on a well defined genetic background including gen es associated with the major histocompatibility complex (MHC) although family studies demonstrate that other genes must be involved as well. Other potential genes include those involved in intrinsic lymphoid hy per-reactivity, for example by preventing programmed cell death. Such examples exist in murine models of SLE, and in this study we provide e vidence that one such controlling protein, bcl-2, is expressed in an i ncreased proportion of both B and T cells in SLE patients. The increas ed expression was not readily related to disease activity measured by the SIS, nor by routine serological markers. This raises the possibili ty that the increased expression of bcl-2 seen in lymphoid cells from SLE patients may be of intrinsic genetic origin rather than being seco ndary to the auto-reactive process. Such increased expression could be expected to interfere with programmed cell death, to produce lymphoid hyper-reactivity and to contribute to the induction and maintenance o f this prototypic systemic autoimmune, disease.