Evidence map›Paper›PMID 38179045›Full record

ReviewFrontiers in immunology2023

ILC2-mediated immune crosstalk in chronic (vascular) inflammation.

Maria Kral, Emiel P C van der Vorst, Alexey Surnov, Christian Weber, Yvonne Döring

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Anti-Inflammatory Interleukins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
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  10. Review
  11. Article
  12. Review
  13. (Multi-) omics studies of ILC2s in inflammation and metabolic diseases.Frontiers in cell and developmental biology · 2024
    Review
  14. Article
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

5 authors at 2 institutions in 3 countries.

Maria KralInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians University Munich, Munich, Germany.
Emiel P C van der VorstInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians University Munich, Munich, Germany.
Alexey SurnovType 1 Diabetes Immunology (TDI), Helmholtz Diabetes Center (HDC), Helmholtz Center Munich, Munich, Germany.
Christian WeberInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians University Munich, Munich, Germany.
Yvonne DöringInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians University Munich, Munich, Germany.
Ludwig-Maximilians-Universität München · DEUniversity Hospital of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Crosstalk between innate and adaptive immunity is pivotal for an efficient immune response and to maintain immune homeostasis under steady state conditions. As part of the innate immune system, type 2 innate lymphoid cells (ILC2s) have emerged as new important regulators of tissue homeostasis and repair by fine-tuning innate-adaptive immune cell crosstalk. ILC2s mediate either pro- or anti-inflammatory immune responses in a context dependent manner. Inflammation has proven to be a key driver of atherosclerosis, resembling the key underlying pathophysiology of cardiovascular disease (CVD). Notably, numerous studies point towards an atheroprotective role of ILC2s e.g., by mediating secretion of type-II cytokines (IL-5, IL-13, IL-9). Boosting these protective responses may be suitable for promising future therapy, although these protective cues are currently incompletely understood. Additionally, little is known about the mechanisms by which chemokine/chemokine receptor signaling shapes ILC2 functions in vascular inflammation and atherosclerosis. Hence, this review will focus on the latest findings regarding the protective and chemokine/chemokine receptor guided interplay between ILC2s and other immune cells like T and B cells, dendritic cells and macrophages in atherosclerosis. Further, we will elaborate on potential therapeutic implications which result or could be distilled from the dialogue of ILC2s with cells of the immune system in cardiovascular diseases.

Indexed as

AtherosclerosisImmunity, InnateChemokinesHumansInflammationLymphocytesReceptors, ChemokineChemokinesReceptors, Chemokineatherosclerosiscardiovascular diseasechemokine receptorsILC2inflammationtissue repair

Identifiers

PMID38179045
PMCPMC10765502
OpenAlexW4390008416

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.