Evidence map›Paper›PMID 27942748›Full record

ReviewCellular and molecular life sciences : CMLS2017

Complement factor H in host defense and immune evasion.

Raffaella Parente, Simon J Clark, Antonio Inforzato, Anthony J Day

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 3% 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

115 citing papers in PubMed, 1 synthesis or guideline pooled it, 190 citations in OpenAlex.

  1. Pooled it
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  5. Suicidality phenotypes reflect both shared and distinct genetic factors.medRxiv : the preprint server for health sciences · 2026
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  8. Frontiers in immunology · 2026
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55 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.

Raffaella ParenteHumanitas Clinical and Research Center, Via Manzoni 56, Rozzano, 20089, Milan, Italy.
Simon J ClarkDivision of Evolution and Genomic Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Oxford Road, Manchester, M13 9PT, UK.
Antonio InforzatoHumanitas Clinical and Research Center, Via Manzoni 56, Rozzano, 20089, Milan, Italy. Antonio.inforzato@humanitasresearch.it.
Anthony J DayWellcome Trust Centre for Cell-Matrix Research, Division of Cell-Matrix Biology and Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Oxford Road, Manchester, M13 9PT, UK. anthony.day@manchester.ac.uk.
Humanitas University · ITUniversity of Manchester · GBWellcome Centre for Cell-Matrix Research · GB

Funding

Medical Research Council G0501816Medical Research Council G0900538Medical Research Council MC_U138274352Medical Research Council MR/K004441/1Medical Research Council MR/K024418/1
6 · The paper itself

Abstract

Complement is the major humoral component of the innate immune system. It recognizes pathogen- and damage-associated molecular patterns, and initiates the immune response in coordination with innate and adaptive immunity. When activated, the complement system unleashes powerful cytotoxic and inflammatory mechanisms, and thus its tight control is crucial to prevent damage to host tissues and allow restoration of immune homeostasis. Factor H is the major soluble inhibitor of complement, where its binding to self markers (i.e., particular glycan structures) prevents complement activation and amplification on host surfaces. Not surprisingly, mutations and polymorphisms that affect recognition of self by factor H are associated with diseases of complement dysregulation, such as age-related macular degeneration and atypical haemolytic uremic syndrome. In addition, pathogens (i.e., non-self) and cancer cells (i.e., altered-self) can hijack factor H to evade the immune response. Here we review recent (and not so recent) literature on the structure and function of factor H, including the emerging roles of this protein in the pathophysiology of infectious diseases and cancer.

Indexed as

Immune EvasionImmunity, InnateAnimalsComplement Factor HDiseaseHumansPolysaccharidesProtein BindingComplement Factor HPolysaccharidesCancer immunologyComplement cascadeComplement factor HGlycan markersInflammatory diseasesInnate immunity

Identifiers

PMID27942748
PMCPMC5378756
OpenAlexW2560499646

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.