Evidence map›Paper›PMID 16809408›Full record

ReviewClinical medicine & research2006

Skewed Th1 responses caused by excessive expression of Txk, a member of the Tec family of tyrosine kinases, in patients with Behcet's disease.

Noboru Suzuki, Kazuhiko Nara, Tomoko Suzuki

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical medicine & research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.9field-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

18 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Behçet syndrome: from pathogenesis to novel therapies.Clinical and experimental medicine · 2016
    Review
  9. Targets for Ibrutinib Beyond B Cell Malignancies.Scandinavian journal of immunology · 2015
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Expression of Th-17 and RORγt mRNA in Behçet's Disease.Medical science monitor : international medical journal of experimental and clinical research · 2011
    Article
  16. Article
  17. Article
  18. 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

3 authors at 2 institutions in 2 countries.

Noboru SuzukiDepartments of Immunology, St. Marianna University School of Medicine, Kawasaki, Kanagawa 216-8511, Japan. n3suzuki@marianna-u.ac.jp
Kazuhiko Nara
Tomoko Suzuki
St. Marianna University School of Medicine · JPNational Archives and Records Administration · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Behcet's disease (BD) is characterized by recurrent attacks of uveitis, oral aphtha, genital ulcers and skin lesions. The etiology and pathogenesis of BD are largely unknown. It has been reported that excessive Th1 cell function is involved in the pathogenesis of BD. Previously, we found that Txk, a member of the Tec family of tyrosine kinases, acts as a Th1 cell-specific transcription factor that is involved in the effector function of Th1 cells. Thus, we studied Th1 cytokine production and Txk expression of T-lymphocytes in patients with BD. Peripheral blood lymphocytes produced excessive Th1-associated cytokines including interferon-gamma (IFN-gamma) and interleukin (IL)-12 in patients with BD. Circulating CD3+ and purified CD4+ T cells expressed excessive Txk protein. The extent of IFN-gamma production by the lymphocytes correlated with the expression of Txk protein in the immunoblotting analysis. The majority of cells infiltrating into the skin lesions of patients with BD expressed IFN-gamma. IL-12 and IL-18 were found in the mononuclear cell aggregates in the skin and intestinal lesions of those with BD. Lymphocytes accumulating in the skin and intestinal lesions expressed higher levels of Txk as compared with other Th2-associated diseases. IFN-gamma, IL-18 and IL-12 detected in skin lesions may induce preferential development of Th1 cells in patients with BD. Collectively, Th1 cells expressing Txk and Th1-associated cytokines may play a critical role in the development of skin and intestinal lesions in patients with BD. This review may serve as a reminder of the importance of excessive Th1 cell function in the pathogenesis of BD and may contribute to the discovery of new molecular targets for the development of a specific therapeutic strategy for BD.

Indexed as

Behcet SyndromeCell DifferentiationCytokinesGene Expression RegulationHumansInterferon-gammaInterleukin-12Interleukin-18Intestinal MucosaIntestinesLymphocytesProtein-Tyrosine KinasesReceptors, CytokineSkinTh1 CellsCytokinesInterferon-gammaInterleukin-12Interleukin-18Protein-Tyrosine KinasesReceptors, CytokineTec protein-tyrosine kinase

Identifiers

PMID16809408
PMCPMC1483892
OpenAlexW2150910359

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.