Evidence map›Paper›PMID 34026337›Full record

ArticleOncoimmunology2021

What role for AHR activation in IL4I1-mediated immunosuppression ?

Flavia Castellano, Armelle Prevost-Blondel, José L Cohen, Valérie Molinier-Frenkel

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Flavia CastellanoINSERM, IMRB, Univ Paris Est Creteil, Creteil, France.
Armelle Prevost-BlondelINSERM, CNRS, Université de Paris, Institut Cochin, PARIS, France.ORCID 0000-0002-7268-5905
José L CohenINSERM, IMRB, Univ Paris Est Creteil, Creteil, France.
Valérie Molinier-FrenkelINSERM, IMRB, Univ Paris Est Creteil, Creteil, France.
Inserm · FRCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The amino-acid catabolizing enzyme Interleukin-4 induced gene 1 (IL4I1) remains poorly characterized despite it is emerging as a pertinent therapeutic target for cancer. IL4I1 is secreted in the synaptic cleft by antigen-presenting cells. It inhibits TCR signaling, modulates naïve T cell differentiation and limits effector T cell proliferation. IL4I1 expression in tumors shapes the tumor microenvironment and impairs the antitumor cytotoxic T cell response, thereby facilitating cancer immune escape. Several mechanisms participate in these effects. Recent data suggest a role of new IL4I1 metabolites in activation of the aryl-hydrocarbon receptor (AHR). Here, we observe that expression of IL4I1 is poorly correlated with that of validated targets of AHR in human cancers. Moreover, dendritic cells do not upregulate AHR target genes in relation with IL4I1 expression

Indexed as

Basic Helix-Loop-Helix ProteinsImmunosuppression TherapyL-Amino Acid OxidaseLymphocyte ActivationReceptors, Aryl HydrocarbonCD8-Positive T-LymphocytesCell DifferentiationHumansAHR protein, humanBasic Helix-Loop-Helix ProteinsIL4I1 protein, humanL-Amino Acid OxidaseReceptors, Aryl HydrocarbonAmino-acid catabolizing enzymearyl-hydrocarbon receptorimmune escapeT cell responsetumor microenvironment

Identifiers

PMID34026337
PMCPMC8118450
OpenAlexW3160091573

What OpenQuestion holds

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Registered trials

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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.