Evidence map›Paper›PMID 41333458›Full record

ArticleFrontiers in immunology2025

Toll-like receptor 1 polymorphism is associated with impaired immune tolerance, dysregulated inflammatory responses to

Morgan A Williams, Sergio A Hernandez, Sheila L Arvikar, Katherine B Sulka, Franc Strle, Christopher C Wells, Tanja Petnicki-Ocwieja, Allen C Steere, Klemen Strle

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Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Morgan A WilliamsDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA, United States.
Sergio A HernandezDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA, United States.
Sheila L ArvikarDivision of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States.
Katherine B SulkaDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA, United States.
Franc StrleDepartment of Infectious Diseases, University Medical Centre Ljubljana, Ljubljana, Slovenia.
Christopher C WellsDepartment of Immunology, Tufts University Graduate School of Biomedical Sciences, Boston, MA, United States.
Tanja Petnicki-OcwiejaDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA, United States.
Allen C SteereDivision of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States.
Klemen StrleDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Clinical presentation of Lyme disease is largely due to host immune response to infection. Previously, we identified a variant (1805GG) in the TLR1 gene, a key immune sensor for Methods: We found that patients with post-infectious Lyme arthritis, a condition characterized by marked persistent synovitis in joints, have a higher frequency of TLR1-1805GG compared to those whose arthritis resolves with antibiotics. To explore the possibility that this genotype-phenotype association was due to excessive inflammation, we then tested the functional impact of TLR1-1805GG on inflammatory responses and immune tolerance in PBMCs with or without this SNP and in THP-1 cell lines lacking TLR1. Results: In response to Conclusions: These results suggest that excessive inflammation in patients with TLR1-1805GG variant appears to be due to immune dysregulation and inability to induce immune tolerance. The findings help explain how early events during the infection may contribute to sustained immune activation after antibiotics and point to the role of TLR1 signaling in immune regulation.

Indexed as

Borrelia burgdorferiImmune ToleranceLyme DiseasePolymorphism, Single NucleotideToll-Like Receptor 1AdultCytokinesFemaleGenetic Predisposition to DiseaseHumansInflammationMaleMiddle AgedTHP-1 CellsCytokinesTLR1 protein, humanToll-Like Receptor 1Borrelia burgdorferiinflammationinnate immune toleranceinnate immunologyLyme arthritisLyme diseasetoll-like receptors

Identifiers

PMID41333458
PMCPMC12665665

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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.