Evidence map›Paper›PMID 24439266›Full record

ArticleImmunity2014

Signaling through the adaptor molecule MyD88 in CD4+ T cells is required to overcome suppression by regulatory T cells.

Dominik Schenten, Simone A Nish, Shuang Yu, Xiting Yan, Heung Kyu Lee, Igor Brodsky, Lesley Pasman, Brian Yordy, F Thomas Wunderlich, Jens C Brüning and 2 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

79 citing papers in PubMed, 118 citations in OpenAlex.

  1. Trial
  2. Review
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  4. Review
  5. Enhancing CAR T-Cell Function with Domains of Innate Immunity Sensors.International journal of molecular sciences · 2025
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  6. The 'TNature reviews. Rheumatology · 2025
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  7. Pyroptosis is involved in the immune microenvironment regulation of unexplained recurrent miscarriage.Mammalian genome : official journal of the International Mammalian Genome Society · 2024
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  10. Harnessing innate immune pathways for therapeutic advancement in cancer.Signal transduction and targeted therapy · 2024
    Review
  11. Article
  12. Article
  13. Review
  14. Immune senescence in aged APP/PS1 mice.NeuroImmune pharmacology and therapeutics · 2023
    Article
  15. Article
  16. Article
  17. Myeloid MyD88 restricts CD8Scientific reports · 2023
    Article
  18. Article
  19. Article
  20. Cytotoxic CD4eLife · 2022
    Article

19 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Dominik SchentenDepartment of Immunobiology, Yale University, New Haven, CT 06519, USA; Howard Hughes Medical Institute, School of Medicine, Yale University, New Haven, CT 06519, USA. Electronic address: dominik.schenten@yale.edu.
Simone A NishDepartment of Immunobiology, Yale University, New Haven, CT 06519, USA; Howard Hughes Medical Institute, School of Medicine, Yale University, New Haven, CT 06519, USA.
Shuang YuDepartment of Immunobiology, Yale University, New Haven, CT 06519, USA; Howard Hughes Medical Institute, School of Medicine, Yale University, New Haven, CT 06519, USA.
Xiting YanDepartment of Biostatistics, Yale School of Public Health, New Haven, CT 06520, USA.
Heung Kyu LeeDepartment of Immunobiology, Yale University, New Haven, CT 06519, USA; Howard Hughes Medical Institute, School of Medicine, Yale University, New Haven, CT 06519, USA.
Igor BrodskyDepartment of Immunobiology, Yale University, New Haven, CT 06519, USA; Howard Hughes Medical Institute, School of Medicine, Yale University, New Haven, CT 06519, USA.
Lesley PasmanDepartment of Immunobiology, Yale University, New Haven, CT 06519, USA; Howard Hughes Medical Institute, School of Medicine, Yale University, New Haven, CT 06519, USA.
Brian YordyDepartment of Immunobiology, Yale University, New Haven, CT 06519, USA.
F Thomas WunderlichMax Planck Institute for Neurological Research, Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), Institute for Genetics, University of Cologne, 50931 Cologne, Germany.
Jens C BrüningMax Planck Institute for Neurological Research, Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), Institute for Genetics, University of Cologne, 50931 Cologne, Germany.
Hongyu ZhaoDepartment of Biostatistics, Yale School of Public Health, New Haven, CT 06520, USA.
Ruslan MedzhitovDepartment of Immunobiology, Yale University, New Haven, CT 06519, USA; Howard Hughes Medical Institute, School of Medicine, Yale University, New Haven, CT 06519, USA. Electronic address: ruslan.medzhitov@yale.edu.
Howard Hughes Medical Institute · USYale University · USCologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEUniversity of Cologne · DE

Funding

Toll Pathway & Control of Adaptive Immune ResponsesR01AI055502 · NIAID · YALE UNIVERSITY · PI MEDZHITOV, RUSLAN · 2003 to 2013
$3.7M
Howard Hughes Medical InstituteNIAID NIH HHS AI055502NIAID NIH HHS R01 AI055502
6 · The paper itself

Abstract

Innate immune recognition controls adaptive immune responses through multiple mechanisms. The MyD88 signaling adaptor operates in many cell types downstream of Toll-like receptors (TLRs) and interleukin-1 (IL-1) receptor family members. Cell-type-specific functions of MyD88 signaling remain poorly characterized. Here, we have shown that the T cell-specific ablation of MyD88 in mice impairs not only T helper 17 (Th17) cell responses, but also Th1 cell responses. MyD88 relayed signals of TLR-induced IL-1, which became dispensable for Th1 cell responses in the absence of T regulatory (Treg) cells. Treg cell-specific ablation of MyD88 had no effect, suggesting that IL-1 acts on naive CD4(+) T cells instead of Treg cells themselves. Together, these findings demonstrate that IL-1 renders naive CD4(+) T cells refractory to Treg cell-mediated suppression in order to allow their differentiation into Th1 cells. In addition, IL-1 was also important for the generation of functional CD4(+) memory T cells.

Indexed as

Adaptive ImmunityAnimalsCells, CulturedImmunity, InnateImmunologic MemoryImmunosuppression TherapyInterleukin-1Interleukin-18MiceMice, Inbred C57BLMice, TransgenicMyeloid Differentiation Factor 88Organ SpecificityReceptors, Interleukin-1Signal TransductionTh17 CellsInterleukin-1Interleukin-18Myeloid Differentiation Factor 88Receptors, Interleukin-1

Identifiers

PMID24439266
PMCPMC4445716
OpenAlexW2039839084

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.