Averil Ma

Keywords inflammaging immune aging fibroblasts adventitia NF-κB TNFAIP3 GZMK+ T cells T cell exhaustion tertiary lymphoid structure ARDS lung Get full text access Log in, subscribe or purchase for full access. References 1. Liu, Z. ∙ Liang, Q. ∙ Ren, Y. ... Immunosenescence: molecular mechanisms and diseases Signal Transduct. Target. Ther. 2023; 8, 200 2. Franceschi, C. ∙ Bonafè, M. ∙ Valensin, S. ... Inflamm-aging. An evolutionary perspective on immunosenescence Ann. N. Y. Acad. Sci. 2000; 908:244-254 3.

Abstract Acute myeloid leukemia (AML) is a deadly hematopoietic malignancy. Although many patients achieve complete remission with standard induction therapy, a combination of cytarabine and anthracycline, ~40% of patients have induction failure. These refractory patients pose a treatment challenge, as they do not respond to salvage therapy or allogeneic stem cell transplant.

Abstract Despite evidence of chronic inflammation in myelodysplastic syndrome (MDS) and cell-intrinsic dysregulation of Toll-like receptor (TLR) signaling in MDS hematopoietic stem and progenitor cells (HSPCs), the mechanisms responsible for the competitive advantage of MDS HSPCs in an inflammatory milieu over normal HSPCs remain poorly defined. Here, we found that chronic inflammation was a determinant for the competitive advantage of MDS HSPCs and for disease progression.