Evidence map›Paper›PMID 28645874›Full record

ArticleClinical immunology (Orlando, Fla.)2017

Attenuated IL-2R signaling in CD4 memory T cells of T1D subjects is intrinsic and dependent on activation state.

Katharine Schwedhelm, Jerill Thorpe, Sara A Murray, Marc Gavin, Cate Speake, Carla Greenbaum, Karen Cerosaletti, Jane Buckner, S Alice Long

Open access · greenAbstract read
In one paragraph

Article in Clinical immunology (Orlando, Fla.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Clinical and experimental treatment of type 1 diabetes.Clinical and experimental immunology · 2022
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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

9 authors at 2 institutions in 1 country.

Katharine SchwedhelmTranslational Research Program, Benaroya Research Institute, Seattle, WA, USA.
Jerill ThorpeTranslational Research Program, Benaroya Research Institute, Seattle, WA, USA.
Sara A MurraySystems Immunology Program, Benaroya Research Institute, Seattle, WA, USA.
Marc GavinTranslational Research Program, Benaroya Research Institute, Seattle, WA, USA.
Cate SpeakeDiabetes Clinical Research Program, Benaroya Research Institute, Seattle, WA, USA.
Carla GreenbaumDiabetes Clinical Research Program, Benaroya Research Institute, Seattle, WA, USA.
Karen CerosalettiTranslational Research Program, Benaroya Research Institute, Seattle, WA, USA.
Jane BucknerTranslational Research Program, Benaroya Research Institute, Seattle, WA, USA.
S Alice LongTranslational Research Program, Benaroya Research Institute, Seattle, WA, USA. Electronic address: along@benaroyaresearch.org.
Benaroya Research InstituteCGIAR · FR

Funding

Defining the role of altered cytokine signaling pathways on autoimmunityU01AI101990 · NIAID · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BUCKNER, JANE HOYT · 2012 to 2016
$12.1M
Defining the functional impact of T1D genes in mouse and man: a unified strategyDP3DK097672 · NIDDK · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BUCKNER, JANE HOYT · 2012 to 2013
$4.4M
Impact of the autoimmunity associated PTPN22 1858TR01AI083455 · NIAID · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BUCKNER, JANE HOYT · 2011 to 2014
$1.7M
Impact of the autoimmunity associated PTPN22 1858TR56AI083455 · NIAID · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BUCKNER, JANE HOYT · 2010 to 2010
$455k
NIAID NIH HHS R01 AI083455NIAID NIH HHS R56 AI083455NIAID NIH HHS U01 AI101990NIDDK NIH HHS DP3 DK097672
6 · The paper itself

Abstract

The IL-2/IL-2R pathway is implicated in type 1 diabetes (T1D). While its role in regulatory T cell (Treg) biology is well characterized, mechanisms that influence IL-2 responses in effector T cells (Teff) are less well understood. We compared IL-2 responses in 95 healthy control and 98 T1D subjects. In T1D, low IL-2 responsiveness was most pronounced in memory Teff. Unlike Treg, CD25 expression did not influence the Teff responses. Reduced IL-2 responses in memory Teff were not rescued by resting, remained lower after activation and proliferation, and were absent in type 2 diabetes. Comparing basal IL-2 responses in resting versus activated cells, memory Teff displayed lower, but more sustained, responses to IL-2 overtime. These results suggest that T1D-associated defects in the Teff compartment are due to intrinsic factors related to activation. Evaluation of both Teff and Treg IL-2R signaling defects in T1D subjects may inform selection of therapies.

Indexed as

AdolescentAdultCase-Control StudiesCD4-Positive T-LymphocytesDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2FemaleHumansInterleukin-2In Vitro TechniquesLymphocyte ActivationMaleMiddle AgedReceptors, Antigen, T-CellReceptors, Interleukin-2Signal TransductionIL2 protein, humanInterleukin-2Receptors, Antigen, T-CellReceptors, Interleukin-2ActivationCD4 T cellIL-2SignalingType 1 diabetes

Identifiers

PMID28645874
PMCPMC5564451
OpenAlexW2688208697

What OpenQuestion holds

Textmetadata
LicenceTDM
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.