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. 2024 Jan 15;9:18. doi: 10.1038/s41392-023-01709-9

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — Schematic illustration showed the mechanism of neddylation pathway in lupus treatment. DN T cells enrichment results in the destruction of immune tolerance with the mass secretion of IFN-γ and IL-17, autoantibody accumulation and the damage of multi-organs, leading to the development of lupus. Inactivation of neddylation pathway (MLN4924 treatment or Ube2m KO in T cells) impaired the neddylation of Cullin1 and then interrupted the ubiquitination of Bim, contributing to the Bim-dependent DN T cell apoptosis, which restores the immune tolerance and finally alleviates lupus symptoms. This figure was created by Figdraw (www.figdraw.com)