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. 2023 Feb 8;14:691. doi: 10.1038/s41467-023-36257-x

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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. 7 — In collagen antibody-induced arthritis (CAIA), macrophages are activated by LPS-mediated TLR signaling and arthritogenic immune complexes, leading to an increased secretion of PAD4. PAD4-mediated citrullination generates antigens that could be recognized by ACPAs. E4 binds to certain group of citrullinated antigens (e.g., ENO1) and forms local immune complexes that preferably interact with the FCGR2B on activated macrophages, delivering regulatory signals to macrophages, promoting IL-10 secretion and reducing osteoclastogenesis. The graph was created and licensed with Biorender.com.