Evidence map›Paper›PMID 33238127›Full record

ArticleCell reports2020

A Two-Step Process of Effector Programming Governs CD4

Adeleye Opejin, Alexey Surnov, Ziva Misulovin, Michelle Pherson, Cindy Gross, Courtney A Iberg, Ian Fallahee, Jessica Bourque, Dale Dorsett, Daniel Hawiger

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Epigenetic Regulation of CD8European journal of immunology · 2025
    Article
  5. Article
  6. Article
  7. An intestinal TNature immunology · 2024
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

10 authors at 1 institution in 1 country.

Adeleye OpejinDepartment of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, MO, USA.
Alexey SurnovDepartment of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, MO, USA.
Ziva MisulovinEdward A. Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of Medicine, St. Louis, MO, USA.
Michelle PhersonEdward A. Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of Medicine, St. Louis, MO, USA.
Cindy GrossDepartment of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, MO, USA.
Courtney A IbergDepartment of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, MO, USA.
Ian FallaheeDepartment of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, MO, USA.
Jessica BourqueDepartment of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, MO, USA.
Dale DorsettEdward A. Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of Medicine, St. Louis, MO, USA.
Daniel HawigerDepartment of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, MO, USA. Electronic address: daniel.hawiger@health.slu.edu.
Saint Louis University · US

Funding

Functions of Hopx in immune tolerance in a model of Multiple SclerosisR01AI113903 · NIAID · SAINT LOUIS UNIVERSITY · PI HAWIGER, DANIEL · 2014 to 2018
$1.9M
NIAID NIH HHS R01 AI113903
6 · The paper itself

Abstract

Various processes induce and maintain immune tolerance, but effector T cells still arise under minimal perturbations of homeostasis through unclear mechanisms. We report that, contrary to the model postulating primarily tolerogenic mechanisms initiated under homeostatic conditions, effector programming is an integral part of T cell fate determination induced by antigenic activation in the steady state. This effector programming depends on a two-step process starting with induction of effector precursors that express Hopx and are imprinted with multiple instructions for their subsequent terminal effector differentiation. Such molecular circuits advancing specific terminal effector differentiation upon re-stimulation include programmed expression of interferon-γ, whose production then promotes expression of T-bet in the precursors. We further show that effector programming coincides with regulatory conversion among T cells sharing the same antigen specificity. However, conventional type 2 dendritic cells (cDC2) and T cell functions of mammalian target of rapamycin complex 1 (mTORC1) increase effector precursor induction while decreasing the proportion of T cells that can become peripheral Foxp3

Indexed as

AnimalsAntigensCD4 AntigensCell DifferentiationImmune ToleranceMiceAntigensCD4 Antigensautoimmunedendritic cellsEAEeffector programmingHopxIFN-γmTORC1steady stateT cellstolerance

Identifiers

PMID33238127
PMCPMC7714042
OpenAlexW3108065600

What OpenQuestion 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 OpenQuestion graph.