Delayed activation-induced T lymphocytes death in aplastic anemia: related with abnormal Fas system.
- Author:
Seong Cheol KIM
1
;
Yoo Hong MIN
;
Seok LEE
;
So Young CHUNG
;
Nae Choon YOO
;
Jung Woon LEE
;
Jee Sook HAHN
;
Yun Woong KO
Author Information
1. Department of Internal Medicine, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
- Publication Type:Original Article ; In Vitro
- MeSH:
Anemia, Aplastic/pathology;
Anemia, Aplastic/immunology*;
Antigens, CD95/blood;
Apoptosis;
Case-Control Studies;
Human;
In Vitro;
Lymphocyte Transformation;
T-Lymphocytes/pathology*;
T-Lymphocytes/immunology*;
Time Factors
- From:The Korean Journal of Internal Medicine
1998;13(1):41-46
- CountryRepublic of Korea
- Language:English
-
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.
