Evidence map›Paper›PMID 26489954›Full record

ReviewThe EMBO journal2015

Complement activation, regulation, and molecular basis for complement-related diseases.

Goran Bajic, Søren E Degn, Steffen Thiel, Gregers R Andersen

Abstract readReview
In one paragraph

Review in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
200citing papers in PubMed, 2 pooled it
12.0field-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

200 citing papers in PubMed, 2 syntheses or guidelines pooled it, 361 citations in OpenAlex.

  1. Pooled it
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  4. Complement-Regulatory Proteins CFHR1 and CFHR3 and Patient Response to Anti-CD20 Monoclonal Antibody Therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
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140 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

4 authors at 1 institution in 2 countries.

Goran BajicDepartment of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark.
Søren E DegnDepartment of Biomedicine, Aarhus University, Aarhus, Denmark Program in Cellular and Molecular Medicine, Children's Hospital, Boston, MA, USA.
Steffen ThielDepartment of Biomedicine, Aarhus University, Aarhus, Denmark st@biomed.au.dk gra@mbg.au.dk.
Gregers R AndersenDepartment of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark st@biomed.au.dk gra@mbg.au.dk.
Aarhus University · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The complement system is an essential element of the innate immune response that becomes activated upon recognition of molecular patterns associated with microorganisms, abnormal host cells, and modified molecules in the extracellular environment. The resulting proteolytic cascade tags the complement activator for elimination and elicits a pro-inflammatory response leading to recruitment and activation of immune cells from both the innate and adaptive branches of the immune system. Through these activities, complement functions in the first line of defense against pathogens but also contributes significantly to the maintenance of homeostasis and prevention of autoimmunity. Activation of complement and the subsequent biological responses occur primarily in the extracellular environment. However, recent studies have demonstrated autocrine signaling by complement activation in intracellular vesicles, while the presence of a cytoplasmic receptor serves to detect complement-opsonized intracellular pathogens. Furthermore, breakthroughs in both functional and structural studies now make it possible to describe many of the intricate molecular mechanisms underlying complement activation and the subsequent downstream events, as well as its cross talk with, for example, signaling pathways, the coagulation system, and adaptive immunity. We present an integrated and updated view of complement based on structural and functional data and describe the new roles attributed to complement. Finally, we discuss how the structural and mechanistic understanding of the complement system rationalizes the genetic defects conferring uncontrolled activation or other undesirable effects of complement.

Indexed as

ProteolysisAnimalsAutocrine CommunicationComplement ActivationHumansInflammationcomplementinflammationinnate immunityproteolytic regulationstructural biology

Identifiers

PMID26489954
PMCPMC4682646
OpenAlexW1835941416

What OpenQuestion holds

Textmetadata
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.