Evidence map›Paper›PMID 33373442›Full record

ArticleThe Journal of experimental medicine2021

Nuclear receptor LXRβ controls fitness and functionality of activated T cells.

Anthony J Michaels, Clarissa Campbell, Regina Bou-Puerto, Alexander Y Rudensky

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Loss of LXRβ Drives CD4Biomedicines · 2026
    Article
  4. Review
  5. Nuclear receptor coregulator NRIP1 R448G modulates T cell gut homing to control intestinal inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Liver X receptor controls follicular helper T cell differentiation via repression of TCF-1.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Anthony J Michaels *Howard Hughes Medical Institute and Immunology Program at Sloan Kettering Institute, Ludwig Center for Cancer Immunotherapy, Memorial Sloan Kettering Cancer Center, New York, NY.
Clarissa Campbell *Howard Hughes Medical Institute and Immunology Program at Sloan Kettering Institute, Ludwig Center for Cancer Immunotherapy, Memorial Sloan Kettering Cancer Center, New York, NY.
Regina Bou-PuertoHoward Hughes Medical Institute and Immunology Program at Sloan Kettering Institute, Ludwig Center for Cancer Immunotherapy, Memorial Sloan Kettering Cancer Center, New York, NY.
Alexander Y RudenskyHoward Hughes Medical Institute and Immunology Program at Sloan Kettering Institute, Ludwig Center for Cancer Immunotherapy, Memorial Sloan Kettering Cancer Center, New York, NY.
Memorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
SELF PEPTIDES BOUND TO MHC CLASS II IN T CELL SELECTIONR01AI034206 · NIAID · UNIVERSITY OF WASHINGTON · PI Alexander Y Rudensky · 1998 to 2026
$6.4M
The Role of Metabolite Sensing in T cell Homeostasis and Tumor ImmunologyF31CA254325 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MICHAELS, ANTHONY · 2020 to 2022
$138k
Howard Hughes Medical InstituteNCI NIH HHS F31 CA254325NCI NIH HHS P30 CA008748NIAID NIH HHS R01 AI034206
6 · The paper itself

Abstract

T cells increase cholesterol biosynthesis upon activation to generate substrates for cellular growth and proliferation. The ubiquitously expressed liver X receptor β (LXRβ) encoded by the Nr1h2 gene is a critical regulator of cholesterol homeostasis in mammalian cells; however, its cell-intrinsic role in T cell biology remains poorly understood. We report that ablation of LXRβ in T cells leads to spontaneous T cell activation and T lymphocytopenia. Unexpectedly, analysis of mixed bone marrow chimeric mice revealed a cell-autonomous survival defect that reduced the fitness of LXRβ-deficient effector T cells, suggesting that the heightened immune activation in mice harboring LXRβ-deficient T cells was due to impaired regulatory T (T reg) cell functionality. Indeed, we found that single-copy deletion of Nr1h2 in T reg cells disrupted activated T reg cell metabolism and fitness and resulted in early-onset fatal autoimmune disease. Our study demonstrated an indispensable requirement for T reg cell-intrinsic LXRβ function in immune homeostasis and provides a basis for immunological therapies through targeting of this receptor.

Indexed as

AnimalsAutoimmune DiseasesCells, CulturedCholesterolFemaleForkhead Transcription FactorsHomeostasisLiver X ReceptorsLymphocyte ActivationMaleMiceMice, Inbred C57BLRadiation ChimeraSignal TransductionT-Lymphocytes, RegulatoryT-Lymphocytopenia, Idiopathic CD4-PositiveCholesterolForkhead Transcription FactorsFoxp3 protein, mouseLiver X ReceptorsNr1h2 protein, mouse

Identifiers

PMID33373442
PMCPMC7774588
OpenAlexW3115237590

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.