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Differential Oncogene and TNF‐α mRNA Expression in Bone Marrow Cells from Systemic Lupus Erythematosus Patients
Author(s) -
AlvaradoDe La Barrera,
AlcocerVarela,
RichaudPatin,
AlarcónSegovia,
Llorente
Publication year - 1998
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1998.00427.x
Subject(s) - bone marrow , oncogene , apoptosis , tumor necrosis factor alpha , medicine , lupus erythematosus , fas ligand , immunology , gene expression , gene , pathology , biology , cell cycle , programmed cell death , antibody , biochemistry
The aim of the study was to investigate the bone marrow expression of genes involved in cell growth and apoptosis in patients with systemic lupus erythematosus (SLE). Spontaneous expression of bcl‐2, bax , c‐ myc , c‐ fos , c‐ jun , p53, Fas and tumour necrosis factor (TNF)‐α by bone marrow cells was measured using either semiquantitative or quantitative reverse transcription polymerase chain reaction in SLE patients ( n = 8) and in eight normal control subjects. The expression of bcl‐2 was found to be higher in SLE patients than in controls. Bone marrow cells from SLE patients showed significant down‐regulation of bax , c‐ myc , c‐ fos and p53 ( P ≤ 0.05), as compared to normal controls. In both SLE patients and controls the expression of c‐ jun and Fas was very low or undetectable. Finally, TNF‐α gene expression was higher in bone marrow samples from SLE patients than in those of controls ( P = 0.01). The abnormal expression of genes regulating cell growth and apoptosis in bone marrow cells from SLE patients may help explain the presence of autoreactive cells in secondary lymphoid organs and peripheral blood of SLE patients.