Evidence map›Paper›PMID 11956247›Full record

ArticleThe Journal of clinical investigation2002

Normal myelopoiesis but abnormal T lymphocyte responses in vitamin D receptor knockout mice.

James O'Kelly, Junichi Hisatake, Yasako Hisatake, June Bishop, Anthony Norman, H Phillip Koeffler

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 149 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Role of Nuclear Receptors in Controlling Erythropoiesis.International journal of molecular sciences · 2022
    Review
  8. Review
  9. Vitamin D3 receptor polymorphisms regulate T cells and T cell-dependent inflammatory diseases.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Association ofMediterranean journal of hematology and infectious diseases · 2020
    Article
  16. Article
  17. Review
  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

6 authors at 3 institutions in 1 country.

James O'KellyDivision of Hematology/Oncology, Cedars-Sinai Medical Center, University of California-Los Angeles School of Medicine, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. okellyj@cshs.org
Junichi Hisatake
Yasako Hisatake
June Bishop
Anthony Norman
H Phillip Koeffler
Cedars-Sinai Medical Center · USUniversity of California, Riverside · USUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The vitamin D receptor (VDR) is a transcription factor that mediates the actions of its ligand, 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)], which can promote monocyte/macrophage differentiation and inhibit proliferation and cytokine production by activated T lymphocytes. In this study, VDR knockout (KO) mice were used to investigate the possible role of VDR in hematopoiesis. The relative number of red and white peripheral blood cells and the percentage of bone marrow macrophages did not differ between VDR KO and wild-type mice. 12-O-tetradecanoylphorbol-13-acetate, but not 1,25(OH)(2)D(3), induced differentiation of bone marrow-committed myeloid stem cells from VDR KO mice to monocytes/macrophages. Production of IL-18, a Th1-promoting cytokine, was reduced in macrophages from these mice. Antigen-stimulated spleen cells from VDR KO mice showed an impaired Th1 cell response and had decreased expression of STAT4, a Th1 cell transcription factor. These results demonstrate the absolute requirement of VDR for 1,25(OH)(2)D(3)-induced monocyte/macrophage differentiation but show that monocyte/macrophage differentiation can occur in the absence of this receptor. The observed reduction in Th1 population in these mutant mice may be explained by a loss of macrophage IL-18 production or a suppression of STAT4 expression by activated splenocytes.

Indexed as

AnimalsCalcitriolCell DifferentiationColony-Forming Units AssayGranulocytesHematopoiesisIn Vitro TechniquesLymphocyte ActivationMacrophagesMiceMice, KnockoutReceptors, CalcitriolTetradecanoylphorbol AcetateTh1 CellsTh2 CellsT-LymphocytesCalcitriolReceptors, CalcitriolTetradecanoylphorbol Acetate

Identifiers

PMID11956247
PMCPMC150940
OpenAlexW2053789854

What OpenQuestion holds

Textmetadata
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.