The bcl-2 proto-oncogene is overexpressed in systemic lupus erythematosus.
J Autoimmun
; 7(5): 623-31, 1994 Oct.
Article
en En
| MEDLINE
| ID: mdl-7840854
Systemic Lupus Erythematosus (SLE) is a disease in which lymphoid hyper-reactivity occurs. Whether this is primary or secondary is not always clear. SLE occurs on a well defined genetic background including genes 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 hyper-reactivity, for example by preventing programmed cell death. Such examples exist in murine models of SLE, and in this study we provide evidence that one such controlling protein, bcl-2, is expressed in an increased proportion of both B and T cells in SLE patients. The increased expression was not readily related to disease activity measured by the SIS, nor by routine serological markers. This raises the possibility that the increased expression of bcl-2 seen in lymphoid cells from SLE patients may be of intrinsic genetic origin rather than being secondary 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 of this prototypic systemic autoimmune disease.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Proto-Oncogenes
/
Proteínas Proto-Oncogénicas
/
Lupus Eritematoso Sistémico
Límite:
Adolescent
/
Adult
/
Female
/
Humans
/
Male
/
Middle aged
Idioma:
En
Revista:
J Autoimmun
Asunto de la revista:
ALERGIA E IMUNOLOGIA
Año:
1994
Tipo del documento:
Article
País de afiliación:
Australia
Pais de publicación:
Reino Unido