Evidence map›Paper›PMID 20231435›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Induction of TGF-beta1 and TGF-beta1-dependent predominant Th17 differentiation by group A streptococcal infection.

Beinan Wang, Thamotharampillai Dileepan, Sarah Briscoe, Kendra A Hyland, Johnthomas Kang, Alexander Khoruts, P Patrick Cleary

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
1.7field-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

58 citing papers in PubMed, 102 citations in OpenAlex.

  1. Trial
  2. Identification of immunostimulatory antigens in Group AProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. NasalJournal of inflammation research · 2026
    Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024
    Review
  9. TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. IL-17A Secreted by Th17 Cells Is Essential for the Host againstJournal of microbiology and biotechnology · 2021
    Article
  18. Review
  19. Review
  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

7 authors at 3 institutions in 2 countries.

Beinan WangDepartment of Microbiology, and Discovery Genomics, Inc, Minneapolis, MN 55413, USA. wangx351@umn.edu
Thamotharampillai Dileepan
Sarah Briscoe
Kendra A Hyland
Johnthomas Kang
Alexander Khoruts
P Patrick Cleary
ID Genomics (United States) · USInstitute of Immunology · HRUniversity of Minnesota Medical Center · US

Funding

T cell immune response to group A streptococci in NALTR01AI059533 · NIAID · UNIVERSITY OF MINNESOTA TWIN CITIES · PI CLEARY, PAUL PATRICK · 2005 to 2008
$1.1M
NIAID NIH HHS AI059533NIAID NIH HHS R01 AI059533
6 · The paper itself

Abstract

Recurrent group A Streptococcus (GAS) tonsillitis and associated autoimmune diseases indicate that the immune response to this organism can be ineffective and pathological. TGF-beta1 is recognized as an essential signal for generation of regulatory T cells (Tregs) and T helper (Th) 17 cells. Here, the impact of TGF-beta1 induction on the T-cell response in mouse nasal-associated lymphoid tissue (NALT) following intranasal (i.n.) infections is investigated. ELISA and TGF-beta1-luciferase reporter assays indicated that persistent infection of mouse NALT with GAS sets the stage for TGF-beta1 and IL-6 production, signals required for promotion of a Th17 immune response. As predicted, IL-17, the Th17 signature cytokine, was induced in a TGF-beta1 signaling-dependent manner in single-cell suspensions of both human tonsils and NALT. Intracellular cytokine staining and flow cytometry demonstrated that CD4(+) IL-17(+) T cells are the dominant T cells induced in NALT by i.n. infections. Moreover, naive mice acquired the potential to clear GAS by adoptive transfer of CD4(+) T cells from immunized IL-17A(+)/(+) mice but not cells from IL-17A(-)/(-) mice. These experiments link specific induction of TGF-beta1 by a bacterial infection to an in vivo Th17 immune response and show that this cellular response is sufficient for protection against GAS. The association of a Th17 response with GAS infection reveals a potential mechanism for destructive autoimmune responses in humans.

Indexed as

Streptococcus pyogenesAnimalsCell DifferentiationCytokinesFemaleHumansImmunity, CellularInterleukin-17Listeria monocytogenesListeriosisLymphoid TissueMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutNasal CavityCytokinesInterleukin-17Transforming Growth Factor beta1

Identifiers

PMID20231435
PMCPMC2851870
OpenAlexW2001553535

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.