Evidence map›Paper›PMID 30149378›Full record

ReviewJournal of innate immunity2018

Complement and Bacterial Infections: From Molecular Mechanisms to Therapeutic Applications.

Dani A C Heesterbeek, Mathieu L Angelier, Richard A Harrison, Suzan H M Rooijakkers

Open access · goldAbstract readReview
In one paragraph

Review in Journal of innate immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

102 citing papers in PubMed, 182 citations in OpenAlex.

  1. Host interactomes ofMicrobiology spectrum · 2026
    Article
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  3. Review
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  7. Review
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  10. Divergent roles for complement components C3 and C4 in controllingbioRxiv : the preprint server for biology · 2025
    Article
  11. Article
  12. A Comprehensive Review of the Bovine Immune Response to Pathogens.International journal of molecular sciences · 2025
    Review
  13. Bioluminescent imaging to investigateInfection and immunity · 2025
    Article
  14. Review
  15. Host complement C3 promotes malaria transmission by killing symbiotic bacteria in the mosquito midgut.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Cell Death and Infection: Implications for Host and Microbe.Advances in experimental medicine and biology · 2025
    Review
  20. Article

42 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 3 institutions in 2 countries.

Dani A C HeesterbeekDepartment of Medical Microbiology, Utrecht University Medical Center, Utrecht, The Netherlands.
Mathieu L AngelierDepartment of Medical Microbiology, Utrecht University Medical Center, Utrecht, The Netherlands.
Richard A HarrisonInstitute of Infection and Immunity, School of Medicine, Cardiff University, Cardiff, United Kingdom.
Suzan H M RooijakkersDepartment of Medical Microbiology, Utrecht University Medical Center, Utrecht, The Netherlandss.h.m.rooijakkers@umcutrecht.nl.
University Medical Center Utrecht · NLCardiff University · GBUtrecht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complement is a complex protein network of plasma, and an integral part of the innate immune system. Complement activation results in the rapid clearance of bacteria by immune cells, and direct bacterial killing via large pore-forming complexes. Here we review important recent discoveries in the complement field, focusing on interactions relevant for the defense against bacteria. Understanding the molecular interplay between complement and bacteria is of great importance for future therapies for infectious and inflammatory diseases. Antibodies that support complement-dependent bacterial killing are of interest for the development of alternative therapies to treat infections with antibiotic-resistant bacteria. Furthermore, a variety of novel therapeutic complement inhibitors have been developed to prevent unwanted complement activation in autoimmune inflammatory diseases. A better understanding of how such inhibitors may increase the risk of bacterial infections is essential if such therapies are to be successful.

Indexed as

AnimalsAnti-Bacterial AgentsAntibody-Dependent Cell CytotoxicityAutoimmune DiseasesBacterial InfectionsComplement ActivationComplement Inactivator ProteinsComplement System ProteinsDrug ResistanceHost-Pathogen InteractionsHumansPhagocytosisAnti-Bacterial AgentsComplement Inactivator ProteinsComplement System ProteinsAntibiotic resistanceAntibody therapyBacteriaComplementEculizumabInfectionsInflammatory diseasesMembrane attack complexNeisseria

Identifiers

PMID30149378
PMCPMC6784045
OpenAlexW2889232296

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.