N-acetyltransferase 10 is implicated in the pathogenesis of cycling T cell-mediated autoimmune and inflammatory disorders in mice

Wen-ping Li, Xin-tao Mao, Jia-huan Xie, Jie-yu Li, Bao-qin Liu, Le-xi Wu, Bing Yang, Yi-yuan Li () and Jin Jin ()
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Wen-ping Li: the Third Affiliated Hospital of Sun Yat-sen University
Xin-tao Mao: the Third Affiliated Hospital of Sun Yat-sen University
Jia-huan Xie: Zhejiang University
Jie-yu Li: the Third Affiliated Hospital of Sun Yat-sen University
Bao-qin Liu: Zhejiang University
Le-xi Wu: College of Medicine Zhejiang University
Bing Yang: Zhejiang University
Yi-yuan Li: Southeast University
Jin Jin: the Third Affiliated Hospital of Sun Yat-sen University

Nature Communications, 2024, vol. 15, issue 1, 1-18

Abstract: Abstract T cell expansion has a crucial function in both autoimmune and chronic inflammatory diseases, with cycling T cells contributing to the pathogenesis of autoimmune diseases by causing uncontrolled immune responses and tissue damage. Yet the regulatory mechanisms governing T cell expansion remain incompletely understood. Here we show that the enzyme N-acetyltransferase 10 (NAT10) regulates T cell activation and proliferation upon antigen stimulation. T cell-specific NAT10 deficiency in mice reduces the number of mature T cells in peripheral lymphoid organs. Mechanistically, NAT10 acetylates RACK1 at K185, preventing subsequent RACK1 K48-linked ubiquitination and degradation. The increased RACK1 stability alters ribosome formation and cellular metabolism, leading to enhanced supply of energy and biosynthetic precursors and, eventually, T cell proliferation. Our findings thus highlight the essential function of NAT10 in T cell self-renewal and metabolism and elucidate NAT10 mode of action for the potential development of novel therapies for immune-related disorders.

Date: 2024
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DOI: 10.1038/s41467-024-53350-x

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