Evidence map›Paper›PMID 22819828›Full record

ReviewFEBS letters2012

Immunoregulatory molecules are master regulators of inflammation during the immune response.

Hortensia de la Fuente, Danay Cibrián, Francisco Sánchez-Madrid

Abstract readReview
In one paragraph

Review in FEBS letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 39 citations in OpenAlex.

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  15. Phenotype and regulation of immunosuppressive Vδ2-expressing γδ T cells.Cellular and molecular life sciences : CMLS · 2014
    Article
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  19. Immune-suppressive properties of the tumor microenvironment.Cancer immunology, immunotherapy : CII · 2013
    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

3 authors at 1 institution in 1 country.

Hortensia de la Fuente *Centro Nacional de Investigaciones Cardiovasculares, Melchor Fernández Almagro, 3, 28029 Madrid, Spain.
Danay Cibrián *Centro Nacional de Investigaciones Cardiovasculares, Melchor Fernández Almagro, 3, 28029 Madrid, Spain.
Francisco Sánchez-MadridCentro Nacional de Investigaciones Cardiovasculares, Melchor Fernández Almagro, 3, 28029 Madrid, Spain.
Spanish National Centre for Cardiovascular Research · ES

Funding

European Research Council 294340
6 · The paper itself

Abstract

The balance between pro- and anti-inflammatory signalling is critical to maintain the immune homeostasis under physiological conditions as well as for the control of inflammation in different pathological settings. Recent progress in the signalling pathways that control this balance has led to the development of novel therapeutic agents for diseases characterized by alterations in the activation/suppression of the immune response. Different molecules have a key role in the regulation of the immune system, including the receptors PD-1 (Programmed cell Death 1), CTLA-4 (Cytotoxic T-Lymphocyte Antigen 4) and galectins; or the intracellular enzyme IDO (indoleamine 2,3-dioxygenase). In addition, other molecules as CD69, AhR (Aryl hydrocarbon Receptor), and GADD45 (Growth Arrest and DNA Damage-inducible 45) family members, have emerged as potential targets for the regulation of the activation/suppression balance of immune cells. This review offers a perspective on well-characterized as well as emergent negative immune regulatory molecules in the context of autoimmune inflammatory diseases.

Indexed as

Adjuvants, ImmunologicInflammationSignal TransductionAdjuvants, Immunologic

Identifiers

PMID22819828
PMCPMC4152724
OpenAlexW2063350197

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.