Open AccessCofilin‐1 participates in the hyperfunction of myeloid dendritic cells in patients with severe aplastic anaemia
Author(s) -
Sun Yingying,
Zhang Yu,
Yu Hong,
Wang Huaquan,
Shao Zonghong,
Liu Chunyan
Publication year - 2022
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.17359
Subject(s) - medicine , myeloid , immunology , hyperfunction , cancer research
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 + and CD8 + T lymphocytes. Collectively, these findings indicate that cofilin‐1 participates in the hyperfunction of mDCs in patients with SAA and that the downregulation of cofilin‐1 in mDCs from patients with SAA could be a novel treatment approach for SAA.