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- W4311141025 abstract "Acute myeloid leukemia (AML) is characterized by an increased proliferation of hematopoietic progenitors or precursors (blasts) of the different myeloid lineages. Studies performed in AML-affected patients revealed a T-cell immunodeficiency, characterized by a decreased number of peripheral T lymphocytes' TRECs and a restricted repertoire. To study thymus dysfunction during AML, we used an AML mouse model in which we previously showed a thymic atrophy notably due to an increased cell death among double-positive (CD4+CD8+) thymocytes. To better understand this massive thymocytes’ loss, we collected ex vivo thymi from control and leukemic mice and immunophenotyped them for cell death. In parallel, we also assessed for the expression of different actors of cell death signaling pathways by RT-qPCR or Western Blotting. When comparing leukemic to control mice, there was a significant increase in the expression of Mlkl gene, phosphorylated MLKL and RIPK3 proteins and TNF-alpha receptors on double-positive (CD4+CD8+) thymocytes. These findings revealed an abnormal cell death of double-positive (CD4+CD8+) thymocytes by necroptosis (in addition to apoptosis) during AML. Such cell death was also observed in vitro using cultured wild-type thymocytes and recombinant TNF-alpha protein in the presence or absence of apoptosis inhibitors. Thus, we demonstrated that TNF-alpha plays a deleterious role in thymic function during AML by contributing to extensive thymocytes’ loss. Further investigations will help to better characterize its impact on the peripheral T-cell repertoire and antigens recognition." @default.
- W4311141025 created "2022-12-23" @default.
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- W4311141025 date "2022-12-01" @default.
- W4311141025 modified "2023-10-01" @default.
- W4311141025 title "221P The role of TNF-alpha in thymus dysfunction during acute myeloid leukemia" @default.
- W4311141025 doi "https://doi.org/10.1016/j.iotech.2022.100332" @default.
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