Evidence map›Paper›PMID 36726757›Full record

ReviewProtein & cell2023

Tinker, tailor, soldier, cell: the role of C-type lectins in the defense and promotion of disease.

James N Arnold, Daniel A Mitchell

Open access · diamondAbstract readReview
In one paragraph

Review in Protein & cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

7 citing papers in PubMed, 11 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

2 authors at 2 institutions in 1 country.

James N ArnoldSchool of Cancer and Pharmaceutical Sciences, King's College London, London SE1 1UL, UK.ORCID 0000-0002-6949-0613
Daniel A MitchellWarwick Medical School, University of Warwick, Coventry CV2 2DX, UK.ORCID 0000-0003-0936-6212
King's College London · GBUniversity of Warwick · GB

Funding

Cancer Research UK DCRPGF\100009
6 · The paper itself

Abstract

C-type lectins (CTLs) represent a large family of soluble and membrane-bound proteins which bind calcium dependently via carbohydrate recognition domains (CRDs) to glycan residues presented on the surface of a variety of pathogens. The deconvolution of a cell's glycan code by CTLs underpins several important physiological processes in mammals such as pathogen neutralization and opsonization, leukocyte trafficking, and the inflammatory response. However, as our knowledge of CTLs has developed it has become apparent that the role of this innate immune family of proteins can be double-edged, where some pathogens have developed approaches to subvert and exploit CTL interactions to promote infection and sustain the pathological state. Equally, CTL interactions with host glycoproteins can contribute to inflammatory diseases such as arthritis and cancer whereby, in certain contexts, they exacerbate inflammation and drive malignant progression. This review discusses the 'dual agent' roles of some of the major mammalian CTLs in both resolving and promoting infection, inflammation and inflammatory disease and highlights opportunities and emerging approaches for their therapeutic modulation.

Indexed as

InflammationLectins, C-TypePolysaccharidesAnimalsHumansMammalsMembrane ProteinsLectins, C-TypeMembrane ProteinsPolysaccharidesarthritiscancerC-type lectinsDC-SIGNinfectionMBLselectins

Identifiers

PMID36726757
PMCPMC9871964
OpenAlexW4288732549

What Socratic 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 Socratic graph.