Evidence map›Paper›PMID 19487419›Full record

ArticleThe Journal of experimental medicine2009

Molecular explanation for the contradiction between systemic Th17 defect and localized bacterial infection in hyper-IgE syndrome.

Yoshiyuki Minegishi, Masako Saito, Masayuki Nagasawa, Hidetoshi Takada, Toshiro Hara, Shigeru Tsuchiya, Kazunaga Agematsu, Masafumi Yamada, Nobuaki Kawamura, Tadashi Ariga and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
131citing papers in PubMed, 1 pooled it
9.1field-weighted citation impact, top 2% 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

131 citing papers in PubMed, 1 synthesis or guideline pooled it, 237 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Single-Cell Profiling Identifies Skin-Resident Memory CD4European journal of immunology · 2026
    Article
  7. Article
  8. Conserved CD4Nature microbiology · 2026
    Article
  9. Hyperimmunoglobulin syndromes: A review of HIGM, HIES, and HIDS.Journal of translational autoimmunity · 2025
    Review
  10. Article
  11. NovelImmune network · 2025
    Article
  12. Frontiers in immunology · 2024
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Human autoantibodies underlying infectious diseases.The Journal of experimental medicine · 2022
    Article
  20. Article

71 more citing papers are in PubMed but not listed here.

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

12 authors at 6 institutions in 1 country.

Yoshiyuki MinegishiDepartment of Immune Regulation, Graduate School, Tokyo Medical and Dental University, Tokyo 113-8519, Japan. yminegishi.mbch@tmd.ac.jp
Masako Saito
Masayuki Nagasawa
Hidetoshi Takada
Toshiro Hara
Shigeru Tsuchiya
Kazunaga Agematsu
Masafumi Yamada
Nobuaki Kawamura
Tadashi Ariga
Ikuya Tsuge
Hajime Karasuyama
Tokyo Medical and Dental University · JPHokkaido University · JPKyushu University · JPFujita Health University · JPShinshu University · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyper-IgE syndrome (HIES) is a primary immunodeficiency characterized by atopic manifestations and susceptibility to infections with extracellular pathogens, typically Staphylococcus aureus, which preferentially affect the skin and lung. Previous studies reported the defective differentiation of T helper 17 (Th17) cells in HIES patients caused by hypomorphic STAT3 mutations. However, the apparent contradiction between the systemic Th17 deficiency and the skin/lung-restricted susceptibility to staphylococcal infections remains puzzling. We present a possible molecular explanation for this enigmatic contradiction. HIES T cells showed impaired production of Th17 cytokines but normal production of classical proinflammatory cytokines including interleukin 1beta. Normal human keratinocytes and bronchial epithelial cells were deeply dependent on the synergistic action of Th17 cytokines and classical proinflammatory cytokines for their production of antistaphylococcal factors, including neutrophil-recruiting chemokines and antimicrobial peptides. In contrast, other cell types were efficiently stimulated with the classical proinflammatory cytokines alone to produce such factors. Accordingly, keratinocytes and bronchial epithelial cells, unlike other cell types, failed to produce antistaphylococcal factors in response to HIES T cell-derived cytokines. These results appear to explain, at least in part, why HIES patients suffer from recurrent staphylococcal infections confined to the skin and lung in contrast to more systemic infections in neutrophil-deficient patients.

Indexed as

Job SyndromeAnimalsAntigens, BacterialAntigens, Fungalbeta-DefensinsChemokinesCytokinesEpithelial CellsHumansInterleukin-8KeratinocytesLung DiseasesReceptors, Interleukin-1Respiratory MucosaStaphylococcal InfectionsStaphylococcal Skin InfectionsAntigens, BacterialAntigens, Fungalbeta-DefensinsChemokinesCytokinesDEFB103A protein, humanDEFB4A protein, humanInterleukin-8Receptors, Interleukin-1STAT3 Transcription Factor

Identifiers

PMID19487419
PMCPMC2715068
OpenAlexW2141987596

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.