Interleukin-2 (alias: IL-2, TCGF, Lymphokine), a type of interleukin, is also a potent signalling molecule in the signalling cascade of the immune-mediated activation of T Lymphocytes leading to the destruction of haematopoietic stem cell (HSC) which is the basis of acquired aplastic anaemia (AAA).
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.
We have investigated the expression of RNA transcripts of hematopoiesis regulatory molecules, viz., macrophage inflammatory protein (MIP)-1<i>α</i>, tumor necrosis factor (TNF)-<i>α</i>, granulocyte colony-stimulating factor (G-CSF), stromal cell-derived factor (SDF)-1<i>α</i>, stem cell factor (SCF), and transforming growth factor (TGF)-<i>β</i> in lipopolysaccharide-induced bone marrow mesenchymal stem cells (BM-MSCs) and levels of their soluble forms in the culture supernatants of BM-MSCs and BM plasma of patients with acquired aplastic anemia (AA) (<i>n</i> = 29) and controls (<i>n</i> = 29).
We have investigated the expression of RNA transcripts of hematopoiesis regulatory molecules, viz., macrophage inflammatory protein (MIP)-1<i>α</i>, tumor necrosis factor (TNF)-<i>α</i>, granulocyte colony-stimulating factor (G-CSF), stromal cell-derived factor (SDF)-1<i>α</i>, stem cell factor (SCF), and transforming growth factor (TGF)-<i>β</i> in lipopolysaccharide-induced bone marrow mesenchymal stem cells (BM-MSCs) and levels of their soluble forms in the culture supernatants of BM-MSCs and BM plasma of patients with acquired aplastic anemia (AA) (<i>n</i> = 29) and controls (<i>n</i> = 29).
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.
The markedly high prevalence of leukocytes lacking HLA-B4002 as a result of either 6pLOH or structural gene mutations, or both, suggests that antigen presentation by hematopoietic stem/progenitor cells to cytotoxic T cells via the HLA-B allele plays a critical role in the pathogenesis of AA.