Evidence map›Paper›PMID 31507535›Full record

ReviewFrontiers in endocrinology2019

The Role of the CXCL12/CXCR4/ACKR3 Axis in Autoimmune Diseases.

Eva M García-Cuesta, César A Santiago, Jesús Vallejo-Díaz, Yasmina Juarranz, José Miguel Rodríguez-Frade, Mario Mellado

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 1 pooled it
9.7field-weighted citation impact, top 1% 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

107 citing papers in PubMed, 1 synthesis or guideline pooled it, 190 citations in OpenAlex.

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47 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Eva M García-CuestaDepartment of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, Madrid, Spain.
César A SantiagoMacromolecular X-Ray Crystallography Unit, Centro Nacional de Biotecnología/CSIC, Madrid, Spain.
Jesús Vallejo-DíazDepartment of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, Madrid, Spain.
Yasmina JuarranzDepartment Cell Biology, Research Institute Hospital 12 de Octubre (i+12), Complutense University of Madrid, Madrid, Spain.
José Miguel Rodríguez-FradeDepartment of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, Madrid, Spain.
Mario MelladoDepartment of Immunology and Oncology, Centro Nacional de Biotecnología/CSIC, Madrid, Spain.
Centro Nacional de Biotecnología · ESResearch Institute Hospital 12 de Octubre · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemokine receptors are members of the G protein-coupled receptor superfamily. These receptors are intimately involved in cell movement, and thus play a critical role in several physiological and pathological situations that require the precise regulation of cell positioning. CXCR4 is one of the most studied chemokine receptors and is involved in many functions beyond leukocyte recruitment. During embryogenesis, it plays essential roles in vascular development, hematopoiesis, cardiogenesis, and nervous system organization. It has been also implicated in tumor progression and autoimmune diseases and, together with CD4, is one of the co-receptors used by the HIV-1 virus to infect immune cells. In contrast to other chemokine receptors that are characterized by ligand promiscuity, CXCR4 has a unique ligand-stromal cell-derived factor-1 (SDF1, CXCL12). However, this ligand also binds ACKR3, an atypical chemokine receptor that modulates CXCR4 functions and is overexpressed in multiple cancer types. The CXCL12/CXCR4/ACKR3 axis constitutes a potential therapeutic target for a wide variety of inflammatory diseases, not only by interfering with cell migration but also by modulating immune responses. Thus far, only one antagonist directed against the ligand-binding site of CXCR4, AMD3100, has demonstrated clinical relevance. Here, we review the role of this ligand and its receptors in different autoimmune diseases.

Indexed as

ACKR3autoimmunitychemokines/chemokine receptorsCXCL12 chemokineCXCR4 = chemokine receptor 4inflammation

Identifiers

PMID31507535
PMCPMC6718456
OpenAlexW2968508798

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.