ArticleInternational journal of hematology2017
TRAIL in CD8+ T cells from patients with severe aplastic anemia.
Article in International journal of hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- TNFSF10 drives hyperactive immune responses via NLRP3 inflammasome and endoplasmic reticulum stress in autoimmune and inflammatory diseases.Journal of advanced research · 2026Article
- Immune suppressive drugs negatively regulate the CD8Heliyon · 2024Article
- A Single-Centre Experience of First-Line Romiplostim and Immunosuppressive Therapy in Patients With Aplastic Anemia.Cureus · 2023Article
- Interferon-gamma and perforin-positive T cells in acquired aplastic anemia: implication in therapeutic response.Clinical and experimental immunology · 2022Article
- Deciphering the Core Metabolites of Fanconi Anemia by Using a Multi-Omics Composite Network.Journal of microbiology and biotechnology · 2022Article
- The Role of lncRNA AF117829.1 in the Immunological Pathogenesis of Severe Aplastic Anaemia.Oxidative medicine and cellular longevity · 2021Article
- [Advances in the pathogenesis of aplastic anaemia].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2019Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Severe aplastic anemia (SAA) is an autoimmune disease caused mainly by activated T lymphocytes. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of TNF family, which can induce apoptosis and play a significant role in the pathogenesis of many autoimmune disorders. In this study, we sought to investigate the role of TRAIL in peripheral CD8+ T cells (CTLs) from SAA patients to clarify the autoimmune mechanisms of bone marrow failure in SAA. The expression of TRAIL and TRAIL-R2 in CTLs from SAA patients and normal controls were determined by flow cytometry, real-time PCR, and western blot. Expression of perforin and granzyme B and apoptosis in CTLs were evaluated by flow cytometry. The expression of TRAIL and TRAIL-R2 in SAA patients was significantly decreased compared with controls; however, there was no statistical difference in TRAIL mRNA expression between the two groups. TRAIL expression in CTLs was negatively correlated with the expression of perforin and granzyme B, and negatively correlated with CTLs apoptosis in SAA patients. The TRAIL pathway may be responsible for abnormal CTL activation in SAA patients. Further study of TRAIL and its receptors may elucidate the pathogenesis of SAA.
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Registered trials
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