Evidence map›Paper›PMID 18490738›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

CD43 regulates Th2 differentiation and inflammation.

Judy L Cannon, Amélie Collins, Purvi D Mody, Diwaker Balachandran, Kammi J Henriksen, Cassandra E Smith, Jiankun Tong, Bryan S Clay, Stephen D Miller, Anne I Sperling

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  5. The mucin-selective protease StcE enables molecular and functional analysis of human cancer-associated mucins.Proceedings of the National Academy of Sciences of the United States of America · 2019
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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

10 authors at 2 institutions in 1 country.

Judy L CannonDepartment of Medicine, Section of Pulmonary and Critical Care Medicine, University of Chicago, Chicago, IL 60637, USA. jlcanno@uchicago.edu
Amélie Collins
Purvi D Mody
Diwaker Balachandran
Kammi J Henriksen
Cassandra E Smith
Jiankun Tong
Bryan S Clay
Stephen D Miller
Anne I Sperling
University of Chicago · USNorthwestern University · US

Funding

IMMUNOREGULATION AND PATHOLOGY OF CHRONIC-RELAPSING EAER01NS026543 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 1988 to 2016
$5.0M
CD43 REGULATION OF IMMUNE RESPONSESR01AI044932 · NIAID · UNIVERSITY OF CHICAGO · PI SPERLING, ANNE I. · 2000 to 2010
$3.1M
NIAID NIH HHS R01 AI044932NIAID NIH HHS R01 AI44932NIAID NIH HHS R01 NS/AI-026543NINDS NIH HHS R01 NS026543
6 · The paper itself

Abstract

CD43 is a highly glycosylated transmembrane protein that regulates T cell activation. CD43(-/-) T cells are hyperproliferative and the cytoplasmic tail of CD43 has been found to be sufficient to reconstitute wild-type proliferation levels, suggesting an intracellular mechanism. In this study, we report that upon TCR ligation CD43(-/-) T cells demonstrated no increase in tyrosine phosphorylation but a decreased calcium flux. Interestingly, CD43(-/-) T cells preferentially differentiated into Th2 cells in vitro, and CD43(-/-) T cells show increased GATA-3 translocation into the nucleus. In vivo, CD43(-/-) mice exhibited increased inflammation in two separate models of Th2-mediated allergic airway disease. In contrast, in Th1-mediated diabetes, nonobese diabetic CD43(-/-) mice did not significantly differ from wild-type mice in disease onset or progression. Th1-induced experimental autoimmune encephalomyelitis to MOG(35-55) was also normal in the CD43(-/-) mice. Nonetheless, the CD43(-/-) mice produced more IL-5 when restimulated with MOG(35-55) in vitro and demonstrated decreased delayed-type hypersensitivity responses. Together, these data demonstrate that although CD43(-/-) T cells preferentially differentiate into Th2 cells, this response is not sufficient to protect against Th1-mediated autoimmune responses.

Indexed as

AnimalsAutoimmunityCalciumCell DifferentiationCell NucleusCell ProliferationCells, CulturedGATA3 Transcription FactorImmunoglobulin EInflammationInterleukin-4Interleukin-5LeukosialinMiceMice, Inbred NODMice, Mutant StrainsCalciumGata3 protein, mouseGATA3 Transcription FactorImmunoglobulin EInterleukin-4Interleukin-5LeukosialinReceptors, Antigen, T-Cell

Identifiers

PMID18490738
PMCPMC2669414
OpenAlexW2122917194

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.