Format

Send to

Choose Destination
Hokkaido Igaku Zasshi. 1997 Jul;72(4):443-55.

[Studies on Fas ligand expression in patients with systemic lupus erythematosus].

[Article in Japanese]

Author information

1
Second Department of Internal Medicine, Hokkaido University School of Medicine, Sapporo, Japan.

Abstract

The Fas/Fas ligand (FasL)-mediated apoptosis may play a role in the induction and maintenance of T cell tolerance. To investigate the role of FasL in the apoptosis of lymphocytes in autoimmune diseases, gene and protein expression of FasL were examined in peripheral blood mononuclear cells (PBMC) from patients with systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA), and from healthy donors by a newly-designed semiquantitative reverse transcription (RT)-PCR and flow cytometry. Although no significant difference in FasL gene expression was obtained among three groups, SLE patients exhibited a wide distribution of the values. In SLE patients, there was a significant correlation between FasL gene expression by PBMC and some clinical parameters including SLE Disease Activity Index (SLEDAI) score, anti-DNA antibody titer and complement titer (CH50). More interestingly, a marked increase in FasL gene expression was observed in untreated SLE patients, whereas a significant decrease was observed in prednisolone-treated SLE patients. Flow cytometric analysis revealed the expression of FasL on T cell subsets from SLE patients and on anti-CD3 mAb-stimulated T cells from healthy donors. In vitro experiments, dexamethasone inhibited FasL gene expression by PBMC from healthy donors in a dose-dependent manner and with time of incubation. These results clearly indicate that FasL is up-regulated in active SLE patients, reflecting in vivo T cell activation, and that corticosteroids directly down-regulate FasL gene expression by human PBMC.

PMID:
9266252
[Indexed for MEDLINE]

Supplemental Content

Loading ...
Support Center