Korean J Intern Med.
1998 Feb;13(1):41-46.
Delayed activation-induced T lymphocytes death in aplastic anemia: related with
abnormal Fas system
- Affiliations
-
- 1Department of Internal Medicine, Severance Hospital, Yonsei University College
of Medicine, Seoul, Korea.
- 2Department of Clinical Pathology, Severance Hospital, Yonsei University College
of Medicine, Seoul, Korea.
Abstract
OBJECTIVES
To quantitate apoptosis and Fas antigen expression of T lymphocytes
by activation in aplastic anemia (AA) and compare with that of normal controls
and completely-recovered AA, and to investigate the apoptotic sensitivity to
anti-fas antibody of activated T lymphocytes in AA. METHODS: We studied the
expression of Fas antigen on fresh T lymphocytes of twenty patients with AA [13
newly diagnosed, 7 recorvered AA after immunosuppressive therapy (IST)], and
investigated the activation-induced cell death (AICD) and Fas expression by
activation [interleukin-2 (200 U/ml) and phytohemagglutinin (50 micrograms/ml)]
in 5 newly-diagnosed AA, 5 normal controls and 5 AA in complete response (CR).
Apoptotic sensitivity to anti-Fas antibody was assessed by the time-course
kinetics of induction of cell death by anti-Fas antibody (500 ng/ml). RESULTS:
There was no significant difference of Fas antigen expression on
freshly-isolated T lymphocytes among newly-diagnosed severe AA, normal control s
and patients with AA in CR after IST. In normal controls, T lymphocytes death
was greatly increased at 3 days of activation, and Fas antigen expression on T
lymphocytes was increased above baseline at day 1 of activation. In contrast, in
newly-diagnosed AA, T lymphocytes showed delayed cell death, which correlated
with a slowed increase of Fas antigen expression by activation. Also, anti-Fa s
antibody sensitivity of activated T lymphocytes was decreased in newly-diagnosed
AA. In completely recovered AA, these abnormal AICD and Fas antigen expressions
by activation were recovered to normal range. CONCLUSIONS: Abnormal AICD plays a
role in the immune pathophysiology of AA, and defective Fas system is involved
in this process.