Evidence map›Paper›PMID 19349465›Full record

ArticleThe Journal of experimental medicine2009

Control of T helper cell differentiation through cytokine receptor inclusion in the immunological synapse.

Roberto A Maldonado, Michelle A Soriano, L Carolina Perdomo, Kirsten Sigrist, Darrell J Irvine, Thomas Decker, Laurie H Glimcher

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 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
0.1field-weighted citation impact, top 49% 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

29 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
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  8. IL-4-producing B cells regulate T helper cell dichotomy in type 1- and type 2-controlled diseases.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  9. Interleukin-35 on B cell and T cell induction and regulation.Journal of inflammation (London, England) · 2017
    Review
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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 4 institutions in 3 countries.

Roberto A MaldonadoDepartment of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
Michelle A Soriano
L Carolina Perdomo
Kirsten Sigrist
Darrell J Irvine
Thomas Decker
Laurie H Glimcher
Harvard University · USImmune Regulation (United Kingdom) · GBMassachusetts Institute of Technology · USUniversity of Vienna · AT

Funding

The function of T Bet in EAEP01NS038037 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI WEINER, HOWARD L · 2000 to 2010
$12.8M
Austrian Science Fund FWF F 2803NINDS NIH HHS P01 NS038037
6 · The paper itself

Abstract

The antigen recognition interface formed by T helper precursors (Thps) and antigen-presenting cells (APCs), called the immunological synapse (IS), includes receptors and signaling molecules necessary for Thp activation and differentiation. We have recently shown that recruitment of the interferon-gamma receptor (IFNGR) into the IS correlates with the capacity of Thps to differentiate into Th1 effector cells, an event regulated by signaling through the functionally opposing receptor to interleukin-4 (IL4R). Here, we show that, similar to IFN-gamma ligation, TCR stimuli induce the translocation of signal transducer and activator of transcription 1 (STAT1) to IFNGR1-rich regions of the membrane. Unexpectedly, STAT1 is preferentially expressed, is constitutively serine (727) phosphorylated in Thp, and is recruited to the IS and the nucleus upon TCR signaling. IL4R engagement controls this process by interfering with both STAT1 recruitment and nuclear translocation. We also show that in cells with deficient Th1 or constitutive Th2 differentiation, the IL4R is recruited to the IS. This observation suggest that the IL4R is retained outside the IS, similar to the exclusion of IFNGR from the IS during IL4R signaling. This study provides new mechanistic cues for the regulation of lineage commitment by mutual immobilization of functionally antagonistic membrane receptors.

Indexed as

Cell DifferentiationHumansInterferon gamma ReceptorInterleukin-4Lymphocyte ActivationModels, ImmunologicalOvalbuminPeptide FragmentsReceptors, Antigen, T-CellReceptors, CytokineReceptors, InterferonReceptors, Interleukin-4SynapsesTh1 CellsT-Lymphocytes, Helper-InducerInterferon gamma ReceptorInterleukin-4OvalbuminPeptide FragmentsReceptors, Antigen, T-CellReceptors, CytokineReceptors, InterferonReceptors, Interleukin-4

Identifiers

PMID19349465
PMCPMC2715121
OpenAlexW1576254943

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.