Evidence map›Paper›PMID 42547779›Full record

Articlenpj metabolic health and disease2026

Overweight and obesity induce Toll-like receptor 2-induced Type I IFN signaling.

Megan Elkins, Amer Al-Musa, Marcos Chiñas, Brian Woods, Aleksandra Bourdine, Lena Ludwig-Radtke, Brenna LaBere, Saddiq Habiballah, Alan A Nguyen, Toshiro K Ohsumi and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in npj metabolic health and disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Megan ElkinsDivision of Immunology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Amer Al-MusaDivision of Immunology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Marcos ChiñasDivision of Immunology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Brian WoodsDivision of Immunology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Aleksandra BourdineDivision of Immunology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Lena Ludwig-RadtkeResearch Group Translational Metabolomics, Core Facility for Metabolomics, Philipps University Marburg, Marburg, Germany.
Brenna LaBereProgram in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge, MA, USA.
Saddiq HabiballahDivision of Immunology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Alan A NguyenDivision of Immunology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Toshiro K OhsumiDivision of Immunology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Maria Gutierrez-ArcelusDivision of Immunology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Amy Fleischman *Division of Endocrinology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
Verena Taudte *Research Group Translational Metabolomics, Core Facility for Metabolomics, Philipps University Marburg, Marburg, Germany.
Janet Chou *Division of Immunology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA. Janet.Chou@childrens.harvard.edu.

Funding

Joint Biology Consortium Resource-based CenterP30AR070253 · BRIGHAM AND WOMEN'S HOSPITAL · 2025 to 2025
$804k
NIH HHS P30AR070253NIH HHS R01DK130465
6 · The paper itself

Abstract

Toll-like receptor 2 (TLR2) is an innate immune receptor linked to obesity primarily via NF-κB activation. Using a mouse model of overnutrition and in vitro TLR2 stimulation of human peripheral blood mononuclear cells, we show that lipids, advanced glycation end products, and low-density lipoproteins extend TLR2 signaling beyond NF-κB to promote Type I IFN production and signaling, establishing the relevance of this pathway to human obesity. This response was abolished by pharmacologic inhibition of the receptor for advanced glycation end products, which recognizes glycated proteins and lipids. In vivo dietary reversal, metformin, and tirzepatide each reduced diet-induced inflammation, but differed in their metabolic effects: dietary reversal reduced weight gain and LDL, tirzepatide reduced weight without lowering LDL, and metformin exerted anti-inflammatory effects independent of weight or LDL. These findings identify TLR2-Type I IFN signaling as a feature of diet-induced inflammation and highlight the diverse immunomodulatory effects of weight-management therapies.

Identifiers

PMID42547779
PMCPMC13434816

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.