Evidence map›Paper›PMID 27211870›Full record

ReviewNature reviews. Nephrology2016

Complement in disease: a defence system turning offensive.

Daniel Ricklin, Edimara S Reis, John D Lambris

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 339 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
339citing papers in PubMed, 3 pooled it
26.0field-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

339 citing papers in PubMed, 3 syntheses or guidelines pooled it, 542 citations in OpenAlex.

  1. Pooled it
  2. Immune cells mediate the causal pathway linking circulating complements to cancer: A Mendelian randomization study.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Pooled it
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  16. Complement system in cancer: friend or foe of immunotherapy.Journal for immunotherapy of cancer · 2026
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279 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

3 authors at 1 institution in 1 country.

Daniel RicklinDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, 401 Stellar Chance, 422 Curie Boulevard, Philadelphia, Pennsylvania 19104, USA.
Edimara S ReisDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, 401 Stellar Chance, 422 Curie Boulevard, Philadelphia, Pennsylvania 19104, USA.
John D LambrisDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, 401 Stellar Chance, 422 Curie Boulevard, Philadelphia, Pennsylvania 19104, USA.
University of Pennsylvania · US

Funding

Role of complement in kidney disorders: from hemodialysis to transportationP01AI068730 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 2007 to 2018
$16.0M
STRUCTURE-FUNCTION ANALYSIS OF DIFFERENT C3 SPECIESR01AI030040 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 1993 to 2016
$4.1M
Novel mechanisms and 'complement-ary' therapy in periodontitisR01DE021685 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2012 to 2016
$2.0M
VIRAL RESPIRATORY PATHOGENS RESEARCH UNIT /VRPRU/-266030040-266030040N01AI030040 · NIAID · UNIVERSITY OF IOWA · PI APICELLA, MICHAEL A. · 2003 to 2006
–
NIAID NIH HHS N01 AI030040NIAID NIH HHS P01 AI068730NIAID NIH HHS R01 AI030040NIDCR NIH HHS R01 DE021685
6 · The paper itself

Abstract

Although the complement system is primarily perceived as a host defence system, a more versatile, yet potentially more harmful side of this innate immune pathway as an inflammatory mediator also exists. The activities that define the ability of the complement system to control microbial threats and eliminate cellular debris - such as sensing molecular danger patterns, generating immediate effectors, and extensively coordinating with other defence pathways - can quickly turn complement from a defence system to an aggressor that drives immune and inflammatory diseases. These host-offensive actions become more pronounced with age and are exacerbated by a variety of genetic factors and autoimmune responses. Complement can also be activated inappropriately, for example in response to biomaterials or transplants. A wealth of research over the past two decades has led to an increasingly finely tuned understanding of complement activation, identified tipping points between physiological and pathological behaviour, and revealed avenues for therapeutic intervention. This Review summarizes our current view of the key activating, regulatory, and effector mechanisms of the complement system, highlighting important crosstalk connections, and, with an emphasis on kidney disease and transplantation, discusses the involvement of complement in clinical conditions and promising therapeutic approaches.

Indexed as

AnimalsAtypical Hemolytic Uremic SyndromeComplement System ProteinsDisease Models, AnimalHumansImmune SystemImmunotherapyKidney DiseasesSignal TransductionThrombotic MicroangiopathiesComplement System Proteins

Identifiers

PMID27211870
PMCPMC4974115
OpenAlexW2397512299

What OpenQuestion holds

Textmetadata
LicenceTDM
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.