Evidence map›Paper›PMID 23576729›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Inducible deletion of the Blimp-1 gene in adult epidermis causes granulocyte-dominated chronic skin inflammation in mice.

Ming-Feng Chiang, Shii-Yi Yang, I-Ying Lin, Jin-Bon Hong, Sung-Jan Lin, Hsia-Yuan Ying, Chun-Ming Chen, Shih-Ying Wu, Fu-Tong Liu, Kuo-I Lin

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. 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
4.1field-weighted citation impact, top 6% 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, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Blimp-1 Upregulation by Multiple LigandsFrontiers in pharmacology · 2022
    Article
  7. Article
  8. Blimp1Nature communications · 2019
    Article
  9. Article
  10. Article
  11. Article
  12. Prdm1 Regulates Thymic Epithelial Function To Prevent Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2017
    Article
  13. Article
  14. Article
  15. Genetically modified laboratory mice with sebaceous glands abnormalities.Cellular and molecular life sciences : CMLS · 2016
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 6 institutions in 1 country.

Ming-Feng ChiangGraduate Institute of Life Sciences, National Defense Medical Center, Taipei 114, Taiwan.
Shii-Yi Yang
I-Ying Lin
Jin-Bon Hong
Sung-Jan Lin
Hsia-Yuan Ying
Chun-Ming Chen
Shih-Ying Wu
Fu-Tong Liu
Kuo-I Lin
Academia Sinica · TWInstitute of Molecular Biology, Academia Sinica · TWNational Taiwan University · TWGenomics Research Center, Academia Sinica · TWNational Defense Medical Center · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

B lymphocyte-induced maturation protein-1 (Blimp-1) is a transcriptional repressor important for the differentiation and function of several types of immune cells. Because skin serves as a physical barrier and acts as an immune sentinel, we investigated whether Blimp-1 is involved in epidermal immune function. We show that Blimp-1 expression is reduced in skin lesions of some human eczema samples and in stimulated primary keratinocytes. Epidermal-specific deletion of PR domain containing 1, with ZNF domain (Prdm1), the gene encoding Blimp-1, in adult mice caused spontaneously inflamed skin characterized by massive dermal infiltration of neutrophils/macrophages and development of chronic inflammation associated with higher levels of cytokines/chemokines, including granulocyte colony-stimulating factor (G-CSF), and enhanced myelopoiesis in bone marrow. Deletion of Prdm1 in the epidermis of adult mice also led to stronger inflammatory reactions in a tape-stripping test and in a disease model of contact dermatitis. The elevated G-CSF produced by keratinocytes after deletion of Prdm1 in vitro was mediated by the transcriptional activation of FBJ osteosarcoma oncogene (Fos) and fos-like antigen 1 (Fosl1). Systemic increases in G-CSF contributed to the inflammatory responses, because deletion of the G-CSF gene [colony stimulating factor 3, (Csf3)] prevented neutrophilia and partially ameliorated the inflamed skin in Prdm1-deficient mice. Our findings indicate a previously unreported function for Blimp-1 in restraining steady-state epidermal barrier immunity.

Indexed as

Gene DeletionAnimalsCytokinesDermatitisDinitrofluorobenzeneEpidermisFlow CytometryFluorescent Antibody TechniqueGranulocyte Colony-Stimulating FactorImmunoblottingKeratinocytesMacrophagesMiceNeutrophil InfiltrationPositive Regulatory Domain I-Binding Factor 1Real-Time Polymerase Chain ReactionCytokinesDinitrofluorobenzeneGranulocyte Colony-Stimulating FactorPositive Regulatory Domain I-Binding Factor 1Prdm1 protein, mouseTranscription Factors

Identifiers

PMID23576729
PMCPMC3631680
OpenAlexW2077337651

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.