Evidence map›Paper›PMID 24713654›Full record

ArticleThe Journal of clinical investigation2014

CXCL11-dependent induction of FOXP3-negative regulatory T cells suppresses autoimmune encephalomyelitis.

Yaniv Zohar, Gizi Wildbaum, Rostislav Novak, Andrew L Salzman, Marcus Thelen, Ronen Alon, Yiftah Barsheshet, Christopher L Karp, Nathan Karin

RetractedErratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 97 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% 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

97 citing papers in PubMed, 1 synthesis or guideline pooled it, 175 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
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  5. Article
  6. ALIGNED Network for rare cerebrovascular diseases: methodology and preliminary results.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
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  11. Engineered chemokines, resistant to cancer-mediated post-transcriptional modifications, as drugs to improve cancer immunotherapy.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Development of DPP-4-resistant CXCL9-Fc and CXCL10-Fc chemokines for effective cancer immunotherapy.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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37 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 3 countries.

Yaniv Zohar
Gizi Wildbaum
Rostislav Novak
Andrew L Salzman
Marcus Thelen
Ronen Alon
Yiftah Barsheshet
Christopher L Karp
Nathan Karin
Rappaport Family Institute for Research in the Medical Sciences · ILCincinnati Children's Hospital Medical Center · USRadikal Therapeutics · USUniversità della Svizzera italiana · CHWeizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A single G protein-coupled receptor (GPCR) can activate multiple signaling cascades based on the binding of different ligands. The biological relevance of this feature in immune regulation has not been evaluated. The chemokine-binding GPCR CXCR3 is preferentially expressed on CD4+ T cells, and canonically binds 3 structurally related chemokines: CXCL9, CXCL10, and CXCL11. Here we have shown that CXCL10/CXCR3 interactions drive effector Th1 polarization via STAT1, STAT4, and STAT5 phosphorylation, while CXCL11/CXCR3 binding induces an immunotolerizing state that is characterized by IL-10(hi) (Tr1) and IL-4(hi) (Th2) cells, mediated via p70 kinase/mTOR in STAT3- and STAT6-dependent pathways. CXCL11 binds CXCR3 with a higher affinity than CXCL10, suggesting that CXCL11 has the potential to restrain inflammatory autoimmunity. We generated a CXCL11-Ig fusion molecule and evaluated its use in the EAE model of inflammatory autoimmune disease. Administration of CXCL11-Ig during the first episode of relapsing EAE in SJL/J mice not only led to rapid remission, but also prevented subsequent relapse. Using GFP-expressing effector CD4+ T cells, we observed that successful therapy was associated with reduced accumulation of these cells at the autoimmune site. Finally, we showed that very low doses of CXCL11 rapidly suppress signs of EAE in C57BL/6 mice lacking functional CXCL11.

Indexed as

AnimalsChemokine CXCL11Encephalomyelitis, Autoimmune, ExperimentalFemaleForkhead Transcription FactorsImmunoglobulin GMiceMice, KnockoutReceptors, CXCR3Recombinant Fusion ProteinsSTAT Transcription FactorsTh1 CellsT-Lymphocytes, RegulatoryChemokine CXCL11Cxcl11 protein, mouseCxcr3 protein, mouseForkhead Transcription FactorsFoxp3 protein, mouseImmunoglobulin GReceptors, CXCR3Recombinant Fusion ProteinsSTAT Transcription Factors

Identifiers

PMID24713654
PMCPMC4001543
OpenAlexW2124907107

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.