---
title: "ARID5B promotes transition from inflammatory to tissue‑destructive fibroblasts in arthritis"
id: "biorxiv-1-arid5b-drives-an-inflammatory-to-destructive-shift-in-pathologic-fibroblast"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-1-arid5b-drives-an-inflammatory-to-destructive-shift-in-pathologic-fibroblast"
content_type: "clinical_feed_article"
specialty: "General"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.08.04.742822v1?rss=1"
published_at: "2026-08-10T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# ARID5B promotes transition from inflammatory to tissue‑destructive fibroblasts in arthritis
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-1-arid5b-drives-an-inflammatory-to-destructive-shift-in-pathologic-fibroblast
- **Specialty:** [General](https://medichelpline.com/clinical-feed/general.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.08.04.742822v1?rss=1)
- **Published At:** 2026-08-10T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- The preprint identifies **ARID5B** as a transcription factor that reprograms activated, inflammatory fibroblasts toward a **migratory** and **invasive** phenotype associated with tissue destruction. - Upregulation of ARID5B in inflammatory fibroblasts leads to its recruitment to both inflammatory and invasive gene loci and to binding interactions with **histone editors**, producing epigenetic changes that alter gene expression. - Functionally, ARID5B activity is reported to **repress pro-inflammatory genes** while **enhancing pro-invasive genes**, producing a net shift from inflammation toward tissue erosion. - Fibroblast-specific overexpression of ARID5B in vivo drove an **inflammatory-to-erosive shift** in arthritis pathology in the model(s) used by the authors, supporting a causal role in disease progression. - The authors propose ARID5B acts as a maladaptive brake on inflammatory activation that paradoxically endows fibroblasts with pathologic invasive properties, mechanistically linking chronic fibroblast-driven inflammation to cartilage and bone damage. - Findings suggest ARID5B and its epigenetic interactions may be potential targets to uncouple fibroblast-driven inflammation from destructive behavior, though therapeutic implications remain exploratory. - This work is a preprint and has not undergone peer review; the manuscript discloses a competing interest for M.B.B. and lists multiple NIH and foundation sources of funding. - Specific experimental details, sample sizes, and full methods are contained in the preprint; where the abstract alone does not report particulars, those details were not reported in the source abstract and should be consulted in the full manuscript.
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Zou, Suppawat Kongthong, Gerald F.M. Watts, Cassandra L. Murphy, Madison L. Fairfield, Alisa A. Mueller, Michael B. Brenner doi: https://doi.org/10.64898/2026.08.04.742822 This article is a preprint and has not been certified by peer review [[what does this mean?](https://www.biorxiv.org/about/FAQ#unrefereed)]. Angela E. Zou 1 Harvard Medical School; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Angela%2BE.%2BZou%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Zou%20AE&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AAngela%2BE.%2BZou%2B) * [ORCID record for Angela E. Zou](http://orcid.org/0000-0002-9709-3121 "Open in new tab") Suppawat Kongthong 1 Harvard Medical School; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Suppawat%2BKongthong%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Kongthong%20S&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ASuppawat%2BKongthong%2B) Gerald F.M. Watts 2 Brigham and Women's Hospital; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Gerald%2BF.M.%2BWatts%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Watts%20GF&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AGerald%2BF.M.%2BWatts%2B) Cassandra L. Murphy 2 Brigham and Women's Hospital; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Cassandra%2BL.%2BMurphy%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Murphy%20CL&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ACassandra%2BL.%2BMurphy%2B) Madison L. Fairfield 2 Brigham and Women's Hospital; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Madison%2BL.%2BFairfield%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Fairfield%20ML&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AMadison%2BL.%2BFairfield%2B) Alisa A. Mueller 3 Stanford University * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Alisa%2BA.%2BMueller%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Mueller%20AA&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AAlisa%2BA.%2BMueller%2B) Michael B. Brenner 2 Brigham and Women's Hospital; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Michael%2BB.%2BBrenner%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Brenner%20MB&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AMichael%2BB.%2BBrenner%2B) * For correspondence: mbrenner@bwh.harvard.edu * [Abstract](https://www.biorxiv.org/content/10.64898/2026.08.04.742822v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5694596/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.08.04.742822v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5694596/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.08.04.742822v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5694596/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.08.04.742822v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5694596/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.08.04.742822v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5694596/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract During inflammatory diseases such as rheumatoid arthritis, fibroblasts prominently drive chronic inflammation and the subsequent destruction of cartilage and bone. The mechanism by which an activated, inflammatory fibroblast acquires tissue destructive behaviors is unknown. Here, we describe ARID5B as a transcription factor that directs inflammatory fibroblasts to become migratory and invasive. Upon upregulation in inflammatory fibroblasts, ARID5B binds to histone editors and localizes to both inflammatory and invasive gene loci, epigenetically repressing pro-inflammatory genes while enhancing expression of pro-invasive genes. Likewise, fibroblast-specific ARID5B overexpression in vivo drives an inflammatory-to-erosive shift in arthritis pathology. Our findings highlight ARID5B as a maladaptive brake on inflammatory fibroblast activation that endows fibroblasts with pathologic invasive properties, thus mechanistically linking fibroblast-driven tissue inflammation to tissue damage. These insights into the regulation of inflammatory and invasive fibroblast pathology may inform successful therapeutic targeting of fibroblasts in inflammatory diseases. ### Competing Interest Statement M.B.B. is on the scientific advisory board of AbbVie and Moderna, a consultant to 4F0 Ventures and a founder of Mestag Therapeutics. ## Funder Information Declared National Institute of Allergy and Infectious Diseases, https://ror.org/043z4tv69, F30AI174699, P01AI148102 National Institute of General Medical Sciences, https://ror.org/04q48ey07, T32GM007753, T32GM144273 National Institute of Arthritis and Musculoskeletal and Skin Diseases, https://ror.org/006zn3t30, K08AR083513, T32AR007530, P30AR070253, R01AR0637039 Rheumatology Research Foundation, https://ror.org/03sdr0263 Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a [CC-BY 4.0 International license](http://creativecommons.org/licenses/by/4.0/). bioRxiv and medRxiv thank the following for their generous financial support: > The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. 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[ Download PDF](https://www.biorxiv.org/content/10.64898/2026.08.04.742822v1.full.pdf) Print/Save Options [Download PDF](https://www.biorxiv.org/content/biorxiv/early/2026/08/10/2026.08.04.742822.full.pdf)Full Text & In-line FiguresXML [More Info](https://www.biorxiv.org/about/FAQ#PrintOptions "More Information on Print/Save Options") [Supplementary Material ](https://www.biorxiv.org/content/10.64898/2026.08.04.742822v1.supplementary-material) [ Email](https://www.biorxiv.org/ "Email this Article") [ Share](https://www.biorxiv.org/) ARID5B drives an inflammatory-to-destructive shift in pathologic fibroblast behavior Angela E. Zou, Suppawat Kongthong, Gerald F.M. Watts, Cassandra L. Murphy, Madison L. Fairfield, Alisa A. Mueller, Michael B. Brenner bioRxiv 2026.08.04.742822; doi: https://doi.org/10.64898/2026.08.04.742822 This article is a preprint and has not been certified by peer review [[what does this mean?](https://www.biorxiv.org/about/FAQ#unrefereed)]. 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