Our results indicate that genetic ATG5 variants contributed to AA, which may facilitate further clarifying the underlying mechanisms of AA and making a patient-tailored medical decision.
In summary, our findings suggest that, although increased circulating IL-18 is a feature of SAA, it may reflect an aberrant immune response but be dispensable to the pathogenesis of AA.
Herein, gene expression analysis identified a significant loss of the SWI/SNF core component SMARCC1, along with ARID1B, ACTL6A, and SMARCD1, in human AA BM CD34<sup>+</sup> HSCs and hematopoietic stem and progenitor cells (HSPCs) compared with normal HSPCs.
Deep sequencing and flow cytometric characterization of expanded effector memory CD8<sup>+</sup>CD57<sup>+</sup> T cells frequently reveals T-cell receptor Vβ oligoclonality and CDR3 homology in acquired aplastic anemia.
Herein, gene expression analysis identified a significant loss of the SWI/SNF core component SMARCC1, along with ARID1B, ACTL6A, and SMARCD1, in human AA BM CD34<sup>+</sup> HSCs and hematopoietic stem and progenitor cells (HSPCs) compared with normal HSPCs.
Herein, gene expression analysis identified a significant loss of the SWI/SNF core component SMARCC1, along with ARID1B, ACTL6A, and SMARCD1, in human AA BM CD34<sup>+</sup> HSCs and hematopoietic stem and progenitor cells (HSPCs) compared with normal HSPCs.
Apart from SMARCD1 loss, we did not observe significant alteration of SWI/SNF expression in MDS HSPCs, indicating SWI/SNF differential expression in AA and MDS.