ArticleJournal of cellular and molecular medicine2022
Cofilin-1 participates in the hyperfunction of myeloid dendritic cells in patients with severe aplastic anaemia.
Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Dysregulated T-cell homeostasis and decreased CD30Heliyon · 2024Article
- Review
- Cofilin-1 participates in the hyperfunction of myeloid dendritic cells in patients with severe aplastic anaemia.Journal of cellular and molecular medicine · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cofilin-1 interacts with actin to regulate cell movement. The importance of cofilin-1 in immunity has been established, and its involvement in a number of autoimmune diseases has been confirmed. However, its role in severe aplastic anaemia (SAA) remains elusive. Thus, the aim of the current study was to investigate the role of cofilin-1 in patients with SAA. Flow cytometry, Western blotting and real-time quantitative reverse transcription-polymerase chain reaction were performed to detect the mRNA and protein expression of cofilin-1 in myeloid dendritic cells (mDCs) from patients with SAA. The expression of cofilin-1 was then suppressed via siRNA, and its effects on mDCs and downstream effector T-cell function were evaluated. Cofilin-1 expression was higher in mDCs from patients with SAA and correlated with routine blood and immune indexes. Moreover, cofilin-1 knockdown in mDCs from patients with SAA reduced their phagocytic capacity, migration capacity, and CD86 expression through F-actin remodelling, downregulating the stimulatory capacity of mDCs on CD4
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