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Deficiency of SATB1 in naive CD4+ T cells alters the 3D chromatin structure and promotes T cell aging [ATAC-seq 2]

ABSTRACT: T cell aging significantly increases the incidence of infections, tumors, and autoimmune diseases in elderly individuals. However, the regulatory factors and molecular mechanisms that influence T cell aging remain unclear. We have previously discovered that the nuclear matrix-binding protein SATB1, a regulatory protein essential for the three-dimensional (3D) genome organization of T cells, plays a pivotal role in T cell activation and the expression of inflammatory genes. Our preliminary results further indicate that during T cell aging, SATB1 expression markedly decreases, resulting in alterations in the 3D genome organization through modulation of CTCF-mediated chromatin interactions. These structural changes subsequently affect the gene expression profile of T cells, thereby promoting the progression of T cell aging. This study aims to further elucidate the molecular mechanisms by which the downregulation of SATB1 remodels the 3D genome organization of T cells, and investigate the protective effects of restoring SATB1 expression on T cell aging. These findings will provide new insights into the mechanisms of T cell aging and may unveil potential therapeutic target for the clinical management of age-related immune decline.

ORGANISM(S): Mus musculus

PROVIDER: GSE298137 | GEO | 2026/08/24

REPOSITORIES: GEO

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Deficiency of SATB1 in naive CD4+ T cells alters the 3D chromatin structure and promotes T cell aging [Hi-C]

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