---
title: "BCAT2-mediated BCAA catabolism sustains interferon-driven macrophage inflammation in rheumatoid ar"
id: "nature-immunology-0-bcat2-links-branched-chain-amino-acids-metabolism-to-interferon-signaling-to"
canonical_url: "https://medichelpline.com/clinical-feed/nature-immunology-0-bcat2-links-branched-chain-amino-acids-metabolism-to-interferon-signaling-to"
content_type: "clinical_feed_article"
specialty: "Infectious Disease"
source_name: "Nature Immunology"
source_url: "https://www.nature.com/articles/s41590-026-02604-5"
published_at: "2026-07-31T09:45:23.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# BCAT2-mediated BCAA catabolism sustains interferon-driven macrophage inflammation in rheumatoid ar
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/nature-immunology-0-bcat2-links-branched-chain-amino-acids-metabolism-to-interferon-signaling-to
- **Specialty:** [Infectious Disease](https://medichelpline.com/clinical-feed/infectious-disease.md)
- **Primary Source:** Nature Immunology
- **Source URL:** [Original Journal Publication](https://www.nature.com/articles/s41590-026-02604-5)
- **Published At:** 2026-07-31T09:45:23.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- The mitochondrial enzyme **BCAT2** links branched-chain amino acid (**BCAA**) catabolism to sustained interferon-driven activation of synovial macrophages in rheumatoid arthritis (RA). - Patients with active RA showed systemic **BCAA** depletion, accumulation of branched-chain ketoacids in synovium, and increased BCAT2 expression in **interferon**-responsive synovial macrophages compared with those in remission. - **Interferon-γ** induces BCAT2 transcription in RA synovial macrophages via the transcription factor **IRF1**. - In human monocyte-derived macrophages, BCAT2-dependent BCAA catabolism raised **mitochondrial ROS**, which inhibited **SHP-1** activity, prolonged **STAT1** and **STAT2** phosphorylation and enhanced inflammatory cytokine production. - Myeloid-specific deletion of Bcat2 in mice reduced disease severity in the collagen antibody-induced arthritis model and suppressed interferon-stimulated gene activation in myeloid cells. - Pharmacological targeting of this pathway with **telmisartan** limited BCAT2-linked macrophage activation and suppressed persistent arthritis in methotrexate-treated mice. - Multi-omics, histology and scRNA-seq approaches underpinned these findings; datasets and source data are available through public repositories cited in the article. - The study identifies BCAT2-dependent amino acid catabolism as a potentially targetable metabolic pathway in autoimmune arthritis and provides mechanistic links between metabolism, redox signaling and sustained interferon responses in synovial macrophages.
## Clinical Analysis & Structured Key Points
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[articles](https://www.nature.com/ni/articles?type=article) 4. article * Article * Published: 31 July 2026 # BCAT2 links branched-chain amino acids metabolism to interferon signaling to sustain macrophage inflammation * [Xiaohui Meng](https://www.nature.com/articles/s41590-026-02604-5#auth-Xiaohui-Meng-Aff1-Aff2-Aff3) [ORCID: orcid.org/0000-0001-6318-6365](https://orcid.org/0000-0001-6318-6365)[1](https://www.nature.com/articles/s41590-026-02604-5#Aff1),[2](https://www.nature.com/articles/s41590-026-02604-5#Aff2),[3](https://www.nature.com/articles/s41590-026-02604-5#Aff3) [na1](https://www.nature.com/articles/s41590-026-02604-5#na1), * [Haihui Han](https://www.nature.com/articles/s41590-026-02604-5#auth-Haihui-Han-Aff1-Aff2-Aff3)[1](https://www.nature.com/articles/s41590-026-02604-5#Aff1),[2](https://www.nature.com/articles/s41590-026-02604-5#Aff2),[3](https://www.nature.com/articles/s41590-026-02604-5#Aff3) [na1](https://www.nature.com/articles/s41590-026-02604-5#na1), * [Wulin You](https://www.nature.com/articles/s41590-026-02604-5#auth-Wulin-You-Aff1-Aff3)[1](https://www.nature.com/articles/s41590-026-02604-5#Aff1),[3](https://www.nature.com/articles/s41590-026-02604-5#Aff3) [na1](https://www.nature.com/articles/s41590-026-02604-5#na1), * [Pengfei Xin](https://www.nature.com/articles/s41590-026-02604-5#auth-Pengfei-Xin-Aff4)[4](https://www.nature.com/articles/s41590-026-02604-5#Aff4) [na1](https://www.nature.com/articles/s41590-026-02604-5#na1), * [Ya Ju](https://www.nature.com/articles/s41590-026-02604-5#auth-Ya-Ju-Aff1-Aff2-Aff3)[1](https://www.nature.com/articles/s41590-026-02604-5#Aff1),[2](https://www.nature.com/articles/s41590-026-02604-5#Aff2),[3](https://www.nature.com/articles/s41590-026-02604-5#Aff3), * [Liangyu Cai](https://www.nature.com/articles/s41590-026-02604-5#auth-Liangyu-Cai-Aff1-Aff2-Aff3)[1](https://www.nature.com/articles/s41590-026-02604-5#Aff1),[2](https://www.nature.com/articles/s41590-026-02604-5#Aff2),[3](https://www.nature.com/articles/s41590-026-02604-5#Aff3), * [Lamei Zhou](https://www.nature.com/articles/s41590-026-02604-5#auth-Lamei-Zhou-Aff1)[1](https://www.nature.com/articles/s41590-026-02604-5#Aff1), * [Sheng Zhong](https://www.nature.com/articles/s41590-026-02604-5#auth-Sheng-Zhong-Aff4-Aff5)[4](https://www.nature.com/articles/s41590-026-02604-5#Aff4),[5](https://www.nature.com/articles/s41590-026-02604-5#Aff5), * [Zhuoyi Hu](https://www.nature.com/articles/s41590-026-02604-5#auth-Zhuoyi-Hu-Aff1-Aff2-Aff3)[1](https://www.nature.com/articles/s41590-026-02604-5#Aff1),[2](https://www.nature.com/articles/s41590-026-02604-5#Aff2),[3](https://www.nature.com/articles/s41590-026-02604-5#Aff3), * [Zhiyu Chen](https://www.nature.com/articles/s41590-026-02604-5#auth-Zhiyu-Chen-Aff1-Aff3)[1](https://www.nature.com/articles/s41590-026-02604-5#Aff1),[3](https://www.nature.com/articles/s41590-026-02604-5#Aff3), * [Wenlei Qin](https://www.nature.com/articles/s41590-026-02604-5#auth-Wenlei-Qin-Aff3)[3](https://www.nature.com/articles/s41590-026-02604-5#Aff3), * [Yanhao Ge](https://www.nature.com/articles/s41590-026-02604-5#auth-Yanhao-Ge-Aff3)[3](https://www.nature.com/articles/s41590-026-02604-5#Aff3), * [Wei Yao](https://www.nature.com/articles/s41590-026-02604-5#auth-Wei-Yao-Aff6-Aff7) [ORCID: orcid.org/0000-0002-1198-1161](https://orcid.org/0000-0002-1198-1161)[6](https://www.nature.com/articles/s41590-026-02604-5#Aff6),[7](https://www.nature.com/articles/s41590-026-02604-5#Aff7), * [Lianbo Xiao](https://www.nature.com/articles/s41590-026-02604-5#auth-Lianbo-Xiao-Aff4-Aff5) [ORCID: orcid.org/0000-0001-9305-0776](https://orcid.org/0000-0001-9305-0776)[4](https://www.nature.com/articles/s41590-026-02604-5#Aff4),[5](https://www.nature.com/articles/s41590-026-02604-5#Aff5) & * … * [Yafeng Zhang](https://www.nature.com/articles/s41590-026-02604-5#auth-Yafeng-Zhang-Aff1-Aff2-Aff3) [ORCID: orcid.org/0009-0008-1492-8009](https://orcid.org/0009-0008-1492-8009)[1](https://www.nature.com/articles/s41590-026-02604-5#Aff1),[2](https://www.nature.com/articles/s41590-026-02604-5#Aff2),[3](https://www.nature.com/articles/s41590-026-02604-5#Aff3) Show authors [_Nature Immunology_](https://www.nature.com/ni) (2026) [Cite this article](https://www.nature.com/articles/s41590-026-02604-5#citeas) [ Save article ](https://www.nature.com/articles/s41590-026-02604-5/save-research?_csrf=IB5YV2pEpLu3lh5NGnc2C8pYqUFR8JKr) [ View saved research ](https://www.nature.com/saved-research) ## Abstract The mechanisms sustaining chronic inflammation in rheumatoid arthritis (RA) remain incompletely understood. Here we show that branched-chain amino acid (BCAA) catabolism, mediated by the mitochondrial enzyme BCAT2, sustained interferon-driven macrophage activation in autoimmune arthritis. Multi-omics and histological analyses of individuals with active RA or sustained remission revealed that active disease was associated with systemic BCAA depletion, synovial branched-chain ketoacid accumulation and elevated BCAT2 expression in interferon-responsive synovial macrophages. Mechanistically, interferon-γ induced BCAT2 transcription through the transcription factor IRF1 in RA synovial macrophages. In human monocyte-derived macrophages, BCAT2-dependent BCAA catabolism elevated mitochondrial reactive oxygen species, which in turn restrained SHP-1 activity, prolonged STAT1 and STAT2 phosphorylation and drove inflammatory cytokine production. Furthermore, myeloid-specific deletion of Bcat2 ameliorated collagen antibody-induced arthritis in mice. Pharmacological targeting of this pathway with telmisartan suppressed persistent arthritis in methotrexate-treated mice. Together, our findings identified BCAT2-dependent amino acid catabolism as a potentially targetable metabolic pathway in autoimmune arthritis. This is a preview of subscription content, [access via your institution](https://wayf.springernature.com?redirect_uri=https%3A%2F%2Fwww.nature.com%2Farticles%2Fs41590-026-02604-5) ## Access options [ Access through your institution ](https://wayf.springernature.com?redirect_uri=https%3A%2F%2Fwww.nature.com%2Farticles%2Fs41590-026-02604-5) Access Nature and 54 other Nature Portfolio journals Get Nature+, our best-value online-access subscription 27,99 € / 30 days cancel any time [Learn more](https://shop.nature.com/products/plus/?region=ROW) Subscribe to this journal Receive 12 print issues and online access 251,40 € per year only 20,95 € per issue [Learn more](https://www.nature.com/ni/subscribe) Buy this article * Purchase on SpringerLink * Instant access to the full article PDF. 39,95 € Prices may be subject to local taxes which are calculated during checkout ### Additional access options: * [Log in](https://idp.nature.com/authorize/natureuser?client_id=grover&redirect_uri=https%3A%2F%2Fwww.nature.com%2Farticles%2Fs41590-026-02604-5) * [Learn about institutional subscriptions](https://www.springernature.com/gp/librarians/licensing/license-options) * [Read our FAQs](https://support.nature.com/en/support/home) * [Contact customer support](https://www.springernature.com/gp/contact) **Fig. 1: Upregulation of BCAT2 in synovial macrophages links BCAA catabolism to active RA.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41590-026-02604-5/MediaObjects/41590_2026_2604_Fig1_HTML.png) **Fig. 2: IFN-associated synovial macrophages and BCAT2 expression in RA.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41590-026-02604-5/MediaObjects/41590_2026_2604_Fig2_HTML.png) **Fig. 3: BCAT2-dependent BCAA catabolism sustains inflammatory activation in macrophages.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41590-026-02604-5/MediaObjects/41590_2026_2604_Fig3_HTML.png) **Fig. 4: BCAT2 promotes STAT signaling through mitochondrial ROS.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41590-026-02604-5/MediaObjects/41590_2026_2604_Fig4_HTML.png) **Fig. 5: Myeloid Bcat2 deficiency ameliorates inflammatory arthritis and suppresses ISG activation.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41590-026-02604-5/MediaObjects/41590_2026_2604_Fig5_HTML.png) **Fig. 6: Telmisartan limits BCAT2-linked macrophage activation.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41590-026-02604-5/MediaObjects/41590_2026_2604_Fig6_HTML.png) ## Data availability Previously published scRNA-seq datasets analyzed in this study are available from the National Genomics Data Center (BioProject [PRJCA013514](http://www.ncbi.nlm.nih.gov/bioproject/?term=PRJCA013514); synovial tissues) and European Molecular Biology Laboratory’s European Bioinformatics Institute (E-MTAB-[8322](http://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-8322/); STMs). scRNA-seq datasets generated in this study from STMs of patients with RA have been deposited in the Genome Sequence Archive for Human at the National Genomics Data Center ([HRA016381](http://ngdc.cncb.ac.cn/gsa-human/browse/HRA016381)) with permission from the Human Genetics Resources Administration of China. scRNA-seq datasets generated in this study from mouse ankle and bone marrow cells have been deposited in the Genome Sequence Archive ([CRA040312](http://bigd.big.ac.cn/gsa/browse/CRA040312)). 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> MedicHelpline content is structured for research, educational, and professional discovery purposes. It does not constitute individual medical advice, clinical diagnosis, or treatment recommendations.
> Always verify dosing, contraindications, and regulatory alerts against official product labeling and primary regulatory sources before clinical decision-making.