ArticleOxidative medicine and cellular longevity2018
PKM2 Is Required to Activate Myeloid Dendritic Cells from Patients with Severe Aplastic Anemia.
Article in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Reconceptualizing Aplastic Anemia-Seed, Worm, Soil.Journal of clinical laboratory analysis · 2026Review
- DNGR-1 signalling limits dendritic cell activation for optimal antigen cross-presentation.The EMBO journal · 2025Article
- Ephedrine attenuates LPS-induced M1 polarization of alveolar macrophages via the PKM2-mediated glycolysis.Toxicology research · 2024Article
- Cellular metabolic basis of altered immunity in the lungs of patients with COVID-19.Medical microbiology and immunology · 2022Article
- Article
- Upregulated expression of leukocyte immunoglobulin-like receptor A3 in patients with severe aplastic anemia.Experimental and therapeutic medicine · 2021Article
- Mechanism of PKM2 affecting cancer immunity and metabolism in Tumor Microenvironment.Journal of Cancer · 2021Review
- Upregulated Expression of Profilin1 on Dendritic Cells in Patients With Severe Aplastic Anemia.Frontiers in immunology · 2021Article
- Effects of Shikonin on the Functions of Myeloid Dendritic Cells in a Mouse Model of Severe Aplastic Anemia.Mediators of inflammation · 2020Article
- [Advances in the pathogenesis of aplastic anaemia].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2019Article
- The prognostic value of PKM2 and its correlation with tumour cell PD-L1 in lung adenocarcinoma.BMC cancer · 2019Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe aplastic anemia (SAA) is an autoimmune disease in which bone marrow failure is mediated by activated myeloid dendritic cells (mDCs) and T lymphocytes. Recent research has identified a strong immunomodulatory effect of pyruvate kinase M2 (PKM2) on dendritic cells in immune-mediated diseases. In this study, we aimed to explore the role of PKM2 in the activation of mDCs in SAA. We observed conspicuously higher levels of PKM2 in mDCs from SAA patients compared to normal controls at both the gene and protein levels. Concurrently, we unexpectedly discovered that after the mDC-specific downregulation of PKM2, mDCs from patients with SAA exhibited weakened phagocytic activity and significantly decreased and shortened dendrites relative to their counterparts from normal controls. The expression levels of the costimulatory molecules CD86 and CD80 were also reduced on mDCs. Our results also suggested that PKM2 knockdown in mDCs reduced the abilities of these cells to promote the activation of CD8+ T cells (CTLs), leading to the decreased secretion of cytotoxic factors by the latter cell type. These findings demonstrate that mDC activation requires an elevated intrinsic PKM2 level and that PKM2 improves the immune status of patients with SAA by enhancing the functions of mDCs and, consequently, CTLs.
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