재생불량성 빈혈의 병태생리에서 Fas 항원과 Apoptosis의 역할
- Alternative Title
- Increased Expression of Fas Antigen and Apoptosis in Aplastic Anemia Bone Marrow Cells
- Abstract
- Background: Clinical observations and laboratory studies have supported an immune basis for most acquired aplastic anemias, with the majority of patients responding to immunosuppressive therapy. Fas, a member of the tumor necrosis factor (TNF) receptor superfamily is a critical downregulator of cellular immune responses. Proinflammatory cytokines like interferon gamma (IFN-${\gamma}$) and TNF-${\alpha}$ can induce Fas expression and render hematopoietic progenitor cells susceptible to Fas-induced growth suppression and apoptosis. Methods: In order to investigate the involvement of apoptosis in the pathogenesis of aplastic anemia (AA), we measured the expression of Fas antigen and caspase-3 on bone marrow (BM) mononuclear cells (MNCs) of AA in the presence or absence of IFN-${\gamma}$, TNF-${\alpha}$, or macrophage inflammatory protein 1-${\alpha}$ (MIP-$1{\alpha}$). Results: We confirmed that AA BM MNCs were more apoptotic and highly expressed Fas antigen than normal donors. Stimulation by IFN-${\gamma}$, TNF-${\alpha}$, or MIP-$1{\alpha}$ increased Fas antigen and caspase-3 expression in AA BM MNCs than BM MNCs of normal donors. Anti-Fas monoclonal antibody enhanced IFN-${\gamma}$, TNF-${\alpha}$, or MIP$1{\alpha}$ mediated caspase-3 expression in BM MNCs of normal donors. Among these three cytokines, IFN-${\gamma}$ enhanced apoptosis most strongly via Fas-caspase-3 pathway. Conclusion: These results suggest that Fas signal pathway may play a role in the pathophysiology of aplastic anemia and negative hematopoietic regulators like IFN-${\gamma}$ can induce apoptosis of bone marrow progenitors in part by Fas induction.
- All Author(s)
- 원종호
; 이남수
; 김숙자
; 정희정
; 이규택
; 박성규
; 백승호
; 김성일
; 홍대식
; 박희숙
- Issued Date
- 2002
- Type
- Article
- Keyword
- Fas antigen; apoptosis; IFN-γ; aplastic anemia
- Publisher
- 대한면역학회
- ISSN
- 1015-6453
; 1598-2629
; 2092-6685
- Citation Title
- Immune Network
- Citation Volume
- 2
- Citation Number
- 1
- Citation Start Page
- 53
- Citation End Page
- 59
- Language(ISO)
- kor
- DOI
- 10.4110/in.2002.2.1.53
- URI
- http://schca-ir.schmc.ac.kr/handle/2022.oak/541
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