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Utilizing single\u2010cell 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\n +<\/jats:sup>\n T cells in AA, driven by reduced ANXA1 expression. This heightened T cell activity promotes adipogenesis in bone marrow\u2010derived mesenchymal stem cells via IFN\u2010\u03b3 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\u2010associated immune microenvironment and bone marrow adiposity.\n \n \n image<\/jats:alt-text>\n <\/jats:graphic>\n <\/jats:boxed-text>\n <\/jats:p>\n <\/jats:sec>\n \n Key points<\/jats:title>\n \n \n \n This study found that ANXA1 is significantly downregulated in AA and provides detailed insights into its critical role in the disease.<\/jats:p>\n <\/jats:list-item>\n \n \n The study demonstrates the excessive activation of CD8\n +<\/jats:sup>\n T cells in the progression of AA.\n <\/jats:p>\n <\/jats:list-item>\n \n \n The research shows that the overexpression of ANXA1 can effectively inhibit the activation of CD8\n +<\/jats:sup>\n T cells.\n <\/jats:p>\n <\/jats:list-item>\n \n The study confirms that overexpression of ANXA1 reduces the secretion of the cytokine IFN\u2010\u03b3, decreases adipogenesis in bone marrow\u2010derived mesenchymal stem cells and may improve AA symptoms.<\/jats:p>\n <\/jats:list-item>\n \n 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