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CD4+ T-Cell Subsets in Aplastic Anemia, Myelodysplastic Syndrome, and Acute Myelogenous Leukemia Patients: a Comparative Analysis. | LitMetric

AI Article Synopsis

  • The study examines the role of CD4+ T-cells in bone marrow failure associated with aplastic anemia (AA), myelodysplastic syndrome (MDS), and acute myelogenous leukemia (AML), noting a lack of prior comparative research.
  • Using flow cytometry and real-time PCR, researchers found distinct differences in CD4+ T-cell subsets among the groups, with higher Th1 and Th17 cells in AA and MDS, while Tregs were decreased in AA but increased in MDS and AML.
  • The findings suggest that an imbalance in CD4+ T-cell populations could significantly contribute to the development of these conditions and associated bone marrow failure.

Article Abstract

Background: Systematic and comparative studies on CD4+ T-lymphocytes in aplastic anemia (AA), myelodysplastic syndrome (MDS), and acute myelogenous leukemia (AML) are scarce. This study aimed to investigate the importance of CD4+ T-cells in bone marrow (BM) failure.

Methods: The proportions of Th1, Th2, Th17, and Treg cells in peripheral blood mononuclear cells (PBMCs) were examined by flow cytometry (FCM). The mRNA expression levels of transcription factors were measured using real-time PCR.

Results: The proportions of Th1, Th17 cells, and Th1/Th2 in the AA group were higher, whereas Th2 and Tregs were lower compared to controls. The proportions of Th17 and Treg cells accompanied by RORγt, and Foxp3 expression were significantly higher in the MDS group. The proportions of Th1, Th17, and Th1/Th2 were higher, whereas Th2 cells and GATA3 expression were significantly lower in MDS-multilineage dysplasia group, than in control group. The proportions of Th1, Th17, and Th1/Th2 were lower in MDS-excess blasts, and AML groups, than in controls, whereas that of Th2 and Treg cells accompanied by GATA3, and Foxp3 expression were significantly higher.

Conclusions: Imbalance in CD4+ T-cell subsets may play a critical role in the pathogenesis and BM failure in the investigated diseases.

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Source
http://dx.doi.org/10.7754/Clin.Lab.2023.221220DOI Listing

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