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. 2024 Oct 10;5:42. doi: 10.1186/s43556-024-00207-w

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© The Author(s) 2024

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — JAK/STAT signaling pathway can be activated or inhibited by inflammatory cytokines to regulate the inflammation of UC. The JAK family (JAK1, JAK2, JAK3, TYK2) binds non-covalently to cytokine receptors, and STATs, as JAK substrates, interact with the tyrosine phosphorylation signaling pathway. JAKs can interact with multiple STATs, which act as the final effectors of signaling, and these combinations can be activated to regulate transcription. Cytokines, including IL-6, IL-12, IL-23, and IL-27, activate the JAK/STAT signaling pathway via the JAK family, regulating the release of Th and Treg cells, thereby influencing UC inflammation. ‘Adapted from “FullTemplateName”, by BioRender.com (CurrentYear). Retrieved from https://app.biorender.com/biorender-templates’