Evidence map›Paper›PMID 34192530›Full record

ArticleCell reports2021

Toll-like receptor 2 induces pathogenicity in Th17 cells and reveals a role for IPCEF in regulating Th17 cell migration.

Kathryne E Marks, Stephanie Flaherty, Kristen M Patterson, Matthew Stratton, Gustavo J Martinez, Joseph M Reynolds

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Gut microbes · 2026
    Article
  2. Naive CD4iScience · 2026
    Article
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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

6 authors at 1 institution in 1 country.

Kathryne E MarksCenter for Cancer Cell Biology, Immunology, and Infection, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA.
Stephanie FlahertyCenter for Cancer Cell Biology, Immunology, and Infection, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA.
Kristen M PattersonCenter for Cancer Cell Biology, Immunology, and Infection, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA.
Matthew StrattonCenter for Cancer Cell Biology, Immunology, and Infection, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA.
Gustavo J MartinezCenter for Cancer Cell Biology, Immunology, and Infection, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA.
Joseph M ReynoldsCenter for Cancer Cell Biology, Immunology, and Infection, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA; Edward Hines Jr. VA Hospital, Hines, IL, USA. Electronic address: joseph.reynolds@rosalindfranklin.edu.
Rosalind Franklin University of Medicine and Science · US

Funding

Molecular regulation of TLR2-mediated autoimmune inflammationR01AI141596 · NIAID · ROSALIND FRANKLIN UNIV OF MEDICINE & SCI · PI REYNOLDS, JOSEPH MICHAEL · 2019 to 2023
$1.9M
Critical roles of endogenous TLR signaling in driving Th17 effector responsesK22AI104941 · NIAID · ROSALIND FRANKLIN UNIV OF MEDICINE & SCI · PI REYNOLDS, JOSEPH MICHAEL · 2013 to 2014
$270k
NIAID NIH HHS K22 AI104941NIAID NIH HHS R01 AI141596
6 · The paper itself

Abstract

Pathogenic Th17 cells drive inflammation in autoimmune disease, yet the molecular programming underlying Th17 cell pathogenicity remains insufficiently understood. Activation of Toll-like receptor 2 (TLR2) increases Th17 cell inflammatory potential, but little is known regarding the mechanistic outcomes of TLR2 signaling in Th17 cells. Here, we demonstrate that TLR2 is comparable to IL-23 in inducing pathogenicity and increasing the migratory capacity of Th17 cells. We perform RNA sequencing of Th17 cells stimulated though the TLR2 pathway and find differential expression of several genes linked with the Th17 genetic program as well as genes not previously associated with pathogenic Th17 cells, including Ipcef1. Enforced expression of Ipcef1 in Th17 cells abolishes the TLR2-dependent increases in migratory capacity and severely impairs the ability of Th17 cells to induce experimental autoimmune encephalomyelitis. This study establishes the importance of the TLR2 signaling pathway in inducing Th17 cell pathogenicity and driving autoimmune inflammation.

Indexed as

Carrier ProteinsCell MovementTh17 CellsToll-Like Receptor 2AnimalsCell DifferentiationCell ProliferationCentral Nervous SystemDown-RegulationEncephalomyelitis, Autoimmune, ExperimentalInterleukin-1betaInterleukin-23Intracellular Signaling Peptides and ProteinsMaleMiceMice, Inbred C57BLCarrier ProteinsInterleukin-1betaInterleukin-23Intracellular Signaling Peptides and ProteinsIpcef1 protein, mouseToll-Like Receptor 2autoimmune diseaseCCL20CCR6EAEIPCEFTh17 cellsToll-like receptor 2Treg cells

Identifiers

PMID34192530
PMCPMC8270556
OpenAlexW3173966570

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.