| First Author | Wang Y | Year | 2020 |
| Journal | Cytotherapy | Volume | 22 |
| Issue | 3 | Pages | 127-134 |
| PubMed ID | 32024607 | Mgi Jnum | J:295753 |
| Mgi Id | MGI:6453543 | Doi | 10.1016/j.jcyt.2020.01.001 |
| Citation | Wang Y, et al. (2020) Interleukin-1beta inhibits normal hematopoietic expansion and promotes acute myeloid leukemia progression via the bone marrow niche. Cytotherapy 22(3):127-134 |
| abstractText | Enhanced interleukin-1beta (IL-1beta) signaling is a common event in patients with acute myeloid leukemia (AML). It was previously demonstrated that chronic IL-1beta exposure severely impaired hematopoietic stem cell (HSC) self-renewal capability in mice and promoted leukemia cell growth in primary AML cells. However, the role of IL-1beta in the murine bone marrow (BM) niche remains unclear. Here, we explored the role of IL-1beta in the BM niche in Il-1r1(-/-) mice, chronic IL-1beta exposure mice and mixed lineage leukemia-AF9 fusion gene (MLL-AF9)-induced AML mice models. We demonstrated that IL-1R1 deficiency did not affect the function of HSCs or niche cells under steady-state conditions or during transplantation. Chronic exposure to IL-1beta decreased the expansion of Il-1r1(-/-) hematopoietic cells in Il-1r1(+/+) recipient mice. These results indicated that IL-1beta exposure impaired the ability of niche cells to support hematopoietic cells. Furthermore, we revealed that IL-1R1 deficiency in niche cells prolonged the survival of MLL-AF9-induced AML mice. The results of our study suggest that inhibition of the IL-1beta/IL-1R1 signaling pathway in the niche might be a non-cell-autonomous therapy strategy for AML. |
