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Delayed activation-induced T lymphocytes death in aplastic anemia: related with abnormal Fas system.

Kim SC, Min YH, Lee S, Chung SY, Yoo NC, Lee JW, Hahn JS, Ko YW - Korean J. Intern. Med. (1998)

Bottom Line: 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).In completely recovered AA, these abnormal AICD and Fas antigen expressions by activation were recovered to normal range.Abnormal AICD plays a role in the immune pathophysiology of AA, and defective Fas system is involved in this process.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, 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 controls 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-Fas 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.

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Related in: MedlinePlus

Gel analysis of genomic DNA extracted from 3-day activated T lymphocytes.
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f5-kjim-13-1-41-7: Gel analysis of genomic DNA extracted from 3-day activated T lymphocytes.

Mentions: In all groups, activated T lymhpocytes showed characteristic DNA fragmentation at day 3 of activation(Fig. 5.)


Delayed activation-induced T lymphocytes death in aplastic anemia: related with abnormal Fas system.

Kim SC, Min YH, Lee S, Chung SY, Yoo NC, Lee JW, Hahn JS, Ko YW - Korean J. Intern. Med. (1998)

Gel analysis of genomic DNA extracted from 3-day activated T lymphocytes.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4531941&req=5

f5-kjim-13-1-41-7: Gel analysis of genomic DNA extracted from 3-day activated T lymphocytes.
Mentions: In all groups, activated T lymhpocytes showed characteristic DNA fragmentation at day 3 of activation(Fig. 5.)

Bottom Line: 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).In completely recovered AA, these abnormal AICD and Fas antigen expressions by activation were recovered to normal range.Abnormal AICD plays a role in the immune pathophysiology of AA, and defective Fas system is involved in this process.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, 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 controls 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-Fas 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.

Show MeSH
Related in: MedlinePlus