Evidence map›Paper›PMID 40350373›Full record

ArticleAnnals of the rheumatic diseases2025

Anti-TFAM antibodies link mitochondrial damage with antiphospholipid syndrome and thrombosis in SLE.

Eduardo Gómez-Bañuelos, Alessandra Ida Celia, Maria Isabel Trejo-Zambrano, Jesus Aureliano Robles-De Anda, Merlin Paz, Shruti Chaturvedi, Fabrizio Conti, Cristiano Alessandri, Eleni Tiniakou, Daniel W Goldman and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of the rheumatic diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Eduardo Gómez-BañuelosDivision of Rheumatology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Alessandra Ida CeliaDivision of Rheumatology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA; Rheumatology Unit, Department of Clinical Internal, Anesthesiological and Cardiovascular Sciences, Sapienza University of Rome, Rome, Italy.
Maria Isabel Trejo-ZambranoDivision of Rheumatology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Jesus Aureliano Robles-De AndaDivision of Rheumatology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Merlin PazDivision of Rheumatology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Shruti ChaturvediDivision of Hematology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Fabrizio ContiRheumatology Unit, Department of Clinical Internal, Anesthesiological and Cardiovascular Sciences, Sapienza University of Rome, Rome, Italy.
Cristiano AlessandriRheumatology Unit, Department of Clinical Internal, Anesthesiological and Cardiovascular Sciences, Sapienza University of Rome, Rome, Italy.
Eleni TiniakouDivision of Rheumatology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Daniel W GoldmanDivision of Rheumatology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Robert A BrodskyDivision of Hematology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Michelle PetriDivision of Rheumatology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Felipe AndradeDivision of Rheumatology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: andrade@jhmi.edu.

Funding

Hopkins Lupus CohortR01AR069572 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI PETRI, MICHELLE A · 2016 to 2020
$3.4M
RNA: Polymerase III specific CD8+ T cells: a mechanistic insight into cancer-induced autoimmunity in sclerodermaK08AR077732 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI TINIAKOU, ELENI · 2021 to 2025
$794k
Transcription factor A mitochondria in SLE pathogenesisR21AI169851 · NIAID · JOHNS HOPKINS UNIVERSITY · PI ANDRADE, FELIPE · 2022 to 2023
$450k
LINE1-ORF0 in SLE pathogenesisR21AI176766 · NIAID · JOHNS HOPKINS UNIVERSITY · PI ANDRADE, FELIPE · 2023 to 2024
$450k
The antigenic origin of anti-dsDNA antibodies in SLER21AI183329 · NIAID · JOHNS HOPKINS UNIVERSITY · PI ANDRADE, FELIPE · 2024 to 2025
$444k
NIAID NIH HHS R21 AI169851NIAID NIH HHS R21 AI176766NIAID NIH HHS R21 AI183329NIAMS NIH HHS K08 AR077732NIAMS NIH HHS R01 AR069572
6 · The paper itself

Abstract

objectivesMitochondria are a source of autoantigens and damage-associated molecular patterns (DAMPs) in systemic lupus erythematosus (SLE). Nucleoids carrying TFAM (transcription factor A, mitochondrial) and mitochondrial DNA (mtDNA) are important DAMPs in SLE. While mtDNA has been associated with anti-double-stranded (ds)DNA antibodies and type I interferon (IFN-I), the immunogenic role of TFAM in SLE pathogenesis is unknown. Here, we characterised the clinical and transcriptional phenotypes linked to anti-TFAM antibodies in SLE.

methodsAnti-TFAM antibodies were discovered in an exploratory sample of 22 SLE patients and 9 healthy controls. To define the prevalence, clinical significance, and associations with transcriptional profiles and IFN levels, anti-TFAM antibodies were detected using enzyme-linked immunosorbent assay (ELISA) in 98 healthy controls and 158 SLE patients. Sera from patients with dermatomyositis, rheumatoid arthritis, and primary antiphospholipid syndrome (PAPS) were also tested.

resultsAnti-TFAM antibodies were discovered in patients with SLE while analysing neutrophil autoantigens and confirmed by ELISA and immunoblotting. One-third of SLE patients (48/158) were positive for anti-TFAM antibodies. Unlike anti-dsDNA antibodies, anti-TFAM antibodies were not associated with disease activity or the IFN signature. Instead, anti-TFAM antibodies were associated with thrombosis, antiphospholipid syndrome (APS) (odds ratio [OR], 2.9 and 5.4, respectively), thrombosis-associated transcriptional profiles, and elevated IFN-III. Anti-TFAM antibodies were also found in PAPS, supporting their role in APS but not SLE pathogenesis. Lupus anticoagulant increased the risk of thrombosis associated with anti-TFAM antibodies (OR, 8.71), indicating they are markers of independent prothrombotic pathways.

conclusionsAnti-TFAM antibodies identify a distinct clinical and transcriptional disease subset associated with mitochondrial damage, thrombosis, and APS in SLE.

Indexed as

Antiphospholipid SyndromeAutoantibodiesDNA-Binding ProteinsLupus Erythematosus, SystemicMitochondriaMitochondrial ProteinsThrombosisTranscription FactorsAdultAutoantigensCase-Control StudiesEnzyme-Linked Immunosorbent AssayFemaleHumansInterferon Type IMaleAutoantibodiesAutoantigensDNA-Binding ProteinsInterferon Type IMitochondrial ProteinsTFAM protein, humanTranscription Factors

Identifiers

PMID40350373
PMCPMC13596704

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.