Evidence map›Paper›PMID 39353255›Full record

ReviewCurrent opinion in immunology2024

The path ahead for understanding Toll-like receptor-driven systemic autoimmunity.

Jessica A Hamerman, Gregory M Barton

Abstract readReview
In one paragraph

Review in Current opinion in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. The SLC15A4-TASL complex is essential for lupus development in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  4. Journal of human immunity · 2026
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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

2 authors.

Jessica A HamermanCenter for Fundamental Immunology, Benaroya Research Institute, Seattle, WA 98101, USA; Department of Immunology, University of Washington, Seattle, WA 98109, USA. Electronic address: JHamerman@benaroyaresearch.org.
Gregory M BartonDivision of Immunology and Molecular Medicine, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA; Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA 94720, USA. Electronic address: barton@berkeley.edu.

Funding

The cell biology of Toll-like receptor 9: a mechanism to prevent autoimmunityR01AI072429 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI Gregory M Barton · 2008 to 2026
$7.6M
BCAP regulation of TLR7/9 signaling in LupusR01AI150178 · NIAID · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI HAMERMAN, JESSICA A · 2020 to 2024
$3.7M
IRF5 and Macrophage Activation Syndrome in systemic Juvenile Idiopathic ArthritisR01AR076242 · NIAMS · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BARNES, BETSY J, HAMERMAN, JESSICA A · 2019 to 2023
$3.3M
Control of Regulatory T Cell Function by Toll-Like Receptor 7R01AI158724 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI BARTON, GREGORY M · 2021 to 2025
$2.8M
Plasmacytoid dendritic cells and IgA autoantibodies in SLER01AI185925 · NIAID · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI Jessica A Hamerman · 2024 to 2026
$2.5M
NIAID NIH HHS R01 AI072429NIAID NIH HHS R01 AI150178NIAID NIH HHS R01 AI158724NIAID NIH HHS R01 AI185925NIAMS NIH HHS R01 AR076242
6 · The paper itself

Abstract

Five mammalian Toll-like receptors (TLR 3, 7, 8, 9, and 13) recognize nucleic acids (NA) and induce signals that control the function of multiple immune cell types and initiate both innate and adaptive immune responses. While these receptors enable recognition of diverse microbial threats, in some instances, they respond inappropriately to self-NA released from host cells and drive the development of autoimmune diseases. Specifically, activation of TLR7 and TLR8 by self-RNA and TLR9 by self-DNA has been linked to development of a collection of systemic autoimmune or autoinflammatory disorders, including systemic lupus erythematosus, systemic juvenile idiopathic arthritis, and macrophage activation syndrome. Here, we discuss recent progress in understanding how these receptors contribute to such diverse clinical phenotypes. We highlight how comparative studies between mice and humans have not only been beneficial in identifying key pathways relevant for disease but also reveal gaps in our understanding of disease mechanisms. We identify several challenges that we hope the field will tackle in the years ahead.

Indexed as

AutoimmunityToll-Like ReceptorsAnimalsAutoimmune DiseasesHumansMiceSignal TransductionToll-Like Receptors

Identifiers

PMID39353255
PMCPMC11863706

What OpenQuestion holds

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Registered trials

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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.