It has great significance for improving the logistics service ability of the Yangtze River economic belt, optimizing the industrial structure of manufacturing industry, and realizing the integrated development of the Yangtze River economic belt to explore the collaborative evolution of logistics industry and manufacturing industry in the Yangtze River economic belt, and identify the leading position of the collaborative development of the two industries, so as to. Based on the Haken Model, this paper summarizes the coevolution law of logistics industry and manufacturing industry in the Yangtze River economic belt through two-stage empirical analysis, and identifies the order parameters of the co-development of logistics industry and manufacturing industry. The results show that the overall degree of coordination between the logistics industry and the manufacturing industry in the Yangtze River economic belt is high. And the order parameter has been changed from manufacturing industry in 2003–2009 to logistics industry in 2010–2017. The gap between regions has been reduced, and the western region has the advantage of post development.

STIP1-homologous U-Box containing protein 1 (STUB1) is involved in the development of immune pathologies and the regulation of T cell. However, the potential role of STUB1 in the pathogenesis of rheumatoid arthritis (RA), especially in the regulation of T cells, remains elusive. Here we show that STUB1 promotes the imbalance of Th17/Treg cells through non-degradative ubiquitination of AHR. Using Western blot and flow cytometry analysis, we observe that the level of STUB1 was increased in RA patients compared with healthy controls. In particular, the expression of STUB1 protein was different in Th17 cells and Treg cells of RA patients. We also demonstrated that STUB1 facilitates Th17/Treg imbalance by up- or down-regulating the expression of STUB1. In a subsequent series of in vitro experiments, we revealed that STUB1 promoted the imbalance of Th17 and Treg cells through non-degradative ubiquitination of AHR. Both knockdown of the AHR expression by siRNA and assays of CYP1A1 enzymatic activity by Ethoxyresorufin-O-Deethylase (EROD) supported this conclusion. Furthermore, we explored the ubiquitination sites of AHR responsible for STUB1-mediated ubiquitination and revealed that STUB1 promotes ubiquitination of AHR via K63 chains. Together, STUB1 may induce the imbalance of Th17/Treg cells via ubiquitination of AHR and serve as a potential therapeutic target for RA.

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