Annexin A1: a key regulator of T cell function and bone marrow adiposity in aplastic anaemia.

Abstract

This study investigates the role of Annexin A1 (ANXA1) in regulating T cell function and its implications in bone marrow adiposity in aplastic anaemia (AA). Utilizing single-cell sequencing analysis, we compared bone marrow tissues from AA patients and healthy individuals, focusing on T cell subgroups and their impact on bone marrow pathology. Our findings reveal a significant activation of CD8+ T cells in AA, driven by reduced ANXA1 expression. This heightened T cell activity promotes adipogenesis in bone marrow-derived mesenchymal stem cells via IFN-γ secretion. Overexpression of ANXA1 was found to suppress this process, suggesting its therapeutic potential in AA treatment. The study highlights ANXA1 as a crucial regulator in the AA-associated immune microenvironment and bone marrow adiposity. KEY POINTS: This study found that ANXA1 is significantly downregulated in AA and provides detailed insights into its critical role in the disease. The study demonstrates the excessive activation of CD8+ T cells in the progression of AA. The research shows that the overexpression of ANXA1 can effectively inhibit the activation of CD8+ T cells. The study confirms that overexpression of ANXA1 reduces the secretion of the cytokine IFN-γ, decreases adipogenesis in bone marrow-derived mesenchymal stem cells and may improve AA symptoms. This research provides new molecular targets for the treatment of AA.