Authors
Xiaojing Wu, Meng Lu, Wenguang Jia, Weixiong Lin, Yunyan He
Published in
PloS one. Volume 21. Issue 9. Pages e0355975. Epub Sep 03, 2026.
Abstract
Despite extensive knowledge of erythropoiesis, the role of interleukin enhancer binding factor 3 (ILF3) in β-thalassemia remains unclear. The aim of this study was to investigate the expression pattern and functional role of ILF3 during erythroid differentiation in β-thalassemia.
(1) Single-cell transcriptomic profiles were constructed based on the GSE133181 dataset (3 healthy controls and 3 β-thalassemia patients). The differential expression of ILF3, transcriptional programs of erythroid subsets, pathway activity, and differentiation trajectory were analyzed. (2) ILF3 was knocked out in K562 cells using sgRNA. Cell proliferation was detected by CCK-8 assay, and apoptosis was measured by Annexin V-APC single staining.
(1) ILF3 was downregulated in the β-thalassemia group, and the proportion of erythroid cells was significantly enriched in ILF3+ cells. (2) ILF3+ erythroid cells highly expressed maturation-related genes and were enriched in cell cycle and metabolic synthesis pathways, while ILF3- cells highly expressed stress-related genes and activated inflammatory stress pathways. (3) Trajectory analysis suggested early arrest of erythroid differentiation in β-thalassemia, with consistently low ILF3 expression throughout the disease group. (4) Knockout of ILF3 promoted apoptosis in K562 cells.
ILF3 is downregulated in β-thalassemia, and its deficiency may contribute to erythroid differentiation arrest and ineffective hematopoiesis by inducing apoptosis and potentially enhancing inflammatory stress.
PMID:
42691027
Bibliographic data and abstract were imported from PubMed on 04 Sep 2026.
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