Evidence map›Paper›PMID 36820828›Full record

ArticleThe Journal of experimental medicine2023

AP-1-independent NFAT signaling maintains follicular T cell function in infection and autoimmunity.

Abhinav Seth, Yoshiyuki Yokokura, Jin-Young Choi, Justin A Shyer, Aurobind Vidyarthi, Joe Craft

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  7. Case Report: NovelFrontiers in immunology · 2025
    Article
  8. Review
  9. Review
  10. Review
  11. 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.

Abhinav SethDepartment of Internal Medicine, Section of Rheumatology, Allergy and Immunology, School of Medicine, Yale University , New Haven, CT, USA.ORCID 0000-0003-0006-3506
Yoshiyuki YokokuraDepartment of Internal Medicine, Section of Rheumatology, Allergy and Immunology, School of Medicine, Yale University , New Haven, CT, USA.ORCID 0000-0002-2875-2031
Jin-Young ChoiDepartment of Internal Medicine, Section of Rheumatology, Allergy and Immunology, School of Medicine, Yale University , New Haven, CT, USA.ORCID 0000-0002-7867-2427
Justin A ShyerDepartment of Immunobiology, School of Medicine, Yale University , New Haven, CT, USA.ORCID 0000-0002-3685-9074
Aurobind VidyarthiDepartment of Internal Medicine, Section of Rheumatology, Allergy and Immunology, School of Medicine, Yale University , New Haven, CT, USA.ORCID 0000-0002-3688-7657
Joe CraftDepartment of Internal Medicine, Section of Rheumatology, Allergy and Immunology, School of Medicine, Yale University , New Haven, CT, USA.ORCID 0000-0002-1368-6756
Yale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
IMMUNE RESPONSES IN LUPUSR37AR040072 · NIAMS · YALE UNIVERSITY · PI CRAFT, JOSEPH EDGAR · 2000 to 2025
$7.4M
Follicular Helper T Cell Function in AutoimmunityR01AR074545 · NIAMS · YALE UNIVERSITY · PI CRAFT, JOSEPH EDGAR · 2019 to 2022
$1.3M
NCATS NIH HHS UL1 TR001863NIAMS NIH HHS R01 AR074545NIAMS NIH HHS R37 AR040072
6 · The paper itself

Abstract

Coordinated gene expression programs enable development and function of T cell subsets. Follicular helper T (Tfh) cells coordinate humoral immune responses by providing selective and instructive cues to germinal center B cells. Here, we show that AP-1-independent NFAT gene expression, a program associated with hyporesponsive T cell states like anergy or exhaustion, is also a distinguishing feature of Tfh cells. NFAT signaling in Tfh cells, maintained by NFAT2 autoamplification, is required for their survival. ICOS signaling upregulates Bcl6 and induces an AP-1-independent NFAT program in primary T cells. Using lupus-prone mice, we demonstrate that genetic disruption or pharmacologic inhibition of NFAT signaling specifically impacts Tfh cell maintenance and leads to amelioration of autoantibody production and renal injury. Our data provide important conceptual and therapeutic insights into the signaling mechanisms that regulate Tfh cell development and function.

Indexed as

AutoimmunityT-Lymphocytes, Helper-InducerAnimalsB-LymphocytesCell DifferentiationGerminal CenterMiceTranscription Factor AP-1Transcription Factor AP-1

Identifiers

PMID36820828
PMCPMC9998660
OpenAlexW4321610851

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.