Evidence map›Paper›PMID 30237800›Full record

ReviewFrontiers in immunology2018

Collectin-11 (CL-11) Is a Major Sentinel at Epithelial Surfaces and Key Pattern Recognition Molecule in Complement-Mediated Ischaemic Injury.

Christopher L Nauser, Mark C Howard, Giorgia Fanelli, Conrad A Farrar, Steven Sacks

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. 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
0.8field-weighted citation impact, top 30% 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, 24 citations in OpenAlex.

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  13. l-Fucose prevention of renal ischaemia/reperfusion injury in Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
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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

5 authors at 2 institutions in 1 country.

Christopher L NauserMRC Centre for Transplantation, School of Immunology and Microbial Sciences, King's College London, Guy's and St. Thomas' NHS Foundation Trust, London, United Kingdom.
Mark C HowardMRC Centre for Transplantation, School of Immunology and Microbial Sciences, King's College London, Guy's and St. Thomas' NHS Foundation Trust, London, United Kingdom.
Giorgia FanelliMRC Centre for Transplantation, School of Immunology and Microbial Sciences, King's College London, Guy's and St. Thomas' NHS Foundation Trust, London, United Kingdom.
Conrad A FarrarMRC Centre for Transplantation, School of Immunology and Microbial Sciences, King's College London, Guy's and St. Thomas' NHS Foundation Trust, London, United Kingdom.
Steven SacksMRC Centre for Transplantation, School of Immunology and Microbial Sciences, King's College London, Guy's and St. Thomas' NHS Foundation Trust, London, United Kingdom.
Guy's and St Thomas' NHS Foundation Trust · GBKing's College London · GB

Funding

Medical Research Council G0600892Medical Research Council G1001141Medical Research Council MR/J004553/1Medical Research Council MR/J006742/1Medical Research Council MR/L012758/1Medical Research Council MR/L020254/1Medical Research Council MR/M007871/1Medical Research Council MR/M012263/1Medical Research Council MR/R010757/1
6 · The paper itself

Abstract

The complement system is a dynamic subset of the innate immune system, playing roles in host defense, clearance of immune complexes and cell debris, and priming the adaptive immune response. Over the last 40 years our understanding of the complement system has evolved from identifying its presence and recognizing its role in the blood to now focusing on understanding the role of local complement synthesis in health and disease. In particular, the local synthesis of complement was found to have an involvement in mediating ischaemic injury, including following transplantation. Recent work on elucidating the triggers of local complement synthesis and activation in renal tissue have led to the finding that Collectin-11 (CL-11) engages with L-fucose at the site of ischaemic stress, namely at the surface of the proximal tubular epithelial cells. What remains unknown is the precise structure of the damage-associated ligand that participates in CL-11 binding and subsequent complement activation. In this article, we will discuss our hypothesis regarding the role of CL-11 as an integral tissue-based pattern recognition molecule which we postulate has a significant contributory role in complement-mediated ischaemic injury.

Indexed as

Kidney TransplantationAnimalsCollectinsComplement ActivationComplement System ProteinsEpithelial CellsHumansIschemiaKidneyReceptors, Pattern RecognitionColec11 protein, humanCollectinsComplement System ProteinsReceptors, Pattern Recognitioncollectin-11complement systeminnate immunitylectin pathwayrenal ischaemiarenal transplantation

Identifiers

PMID30237800
PMCPMC6136055
OpenAlexW2889767272

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.