Cited by 87Complement system in diseasesCoagulation, Bradykinin, Polyphosphates, and AngioedemaBiomarkers in Disease Mechanisms

Self‐nonself discrimination by the complement system

Open access
Meri, Seppo·2016·FEBS Letters

Abstract

The alternative pathway ( AP ) of complement can recognize nonself structures by only two molecules, C3b and factor H. The AP deposits C3b covalently on nonself structures via an amplification system. The actual discrimination is performed by factor H, which has binding sites for polyanions (sialic acids, glycosaminoglycans, phospholipids). This robust recognition of ‘self’ protects our own intact viable cells and tissues, while activating structures are recognized by default. Foreign targets are opsonized for phagocytosis or killed. Mutations in factor H predispose to severe diseases. In hemolytic uremic syndrome, they promote complement attack against blood cells and vascular endothelial cells and lead, for example, to kidney and brain damage. Even pathogens can exploit factor H. In fact, the ability to bind factor H discriminates most pathogenic microbes from nonpathogenic ones.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1002/1873-3468.12284

Cites

136 of 136 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Complement activity is tightly controlled by soluble and surface-bound regulatory proteins to avoid unnecessary damage to host tissues and organs.

    “Because the complement cascade leads to generation of highly potent inflammatory molecules, its activity is tightly regulated by a variety of soluble and surface-bound regulatory proteins, thus preventing unnecessary damage to host tissues and organs.80,81”

    From Innate immune sensing of adeno-associated virus vectors (2024) · cites this paper as [81]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 1

  1. Kraiczy P, Skerka C, Kirschfink M, Brade V and Zipfel PF (2001) Immune evasion of Borrelia 2433 FEBS Letters 590 (2016) 2418-2434 ª 2016 Federation of European Biochemical Societies S. Meri Self-nonself discrimination by the complement system 18733468, 2016, 15, Downloaded from https://febs.onlinelibrary.wiley.com/doi/10.1002/1873-3468.12284, Wiley Online Library on [31/08/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License burgdorferi by acquisition of human complement regulators FHL-1/reconectin and factor H. Eur J Immunol 31, 1674-1684. 123

Cited by

Sorted by citations

Authors
Meri, S.
Affiliations
University of Helsinki (FI)
Corresponding author
Meri, Seppo
Venue
FEBS Letters
Publisher
Wiley
Published
2016-07-19
Volume
590
Issue
15
Pages
2418-2434
ISSN
  • 0014-5793 (ISSN-L)
  • 1873-3468
OpenAlex
W2466150469
Cited by
87
References
136
Citations by year
2026: 4 · 2025: 11 · 2024: 7 · 2023: 3 · 2022: 13 · 2021: 4 · 2020: 14 · 2019: 9 · 2018: 7 · 2017: 11 · 2016: 4
FWCI
1.00
Type
journal article
Language
en
Open access
Locations
  • FEBS Letters (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Suomen Akatemia
  • Sigrid Juséliuksen Säätiö
  • Signe ja Ane Gyllenbergin Säätiö
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
  • Health Sciences › Medicine › Genetics › Coagulation, Bradykinin, Polyphosphates, and Angioedema
  • Life Sciences › Immunology and Microbiology › Immunology › Biomarkers in Disease Mechanisms
Keywords
complement system, alternative complement pathway, self/non-self discrimination, complement factor H, C3b, opsonization, sialic acid, polyanion binding, hemolytic uremic syndrome, factor H mutation, pathogen recognition
MeSH terms
Bacteria, Binding Sites, Brain Injuries, Complement Pathway, Alternative, Complement C3b, Glycosaminoglycans, Hemolytic-Uremic Syndrome, Humans, Mutation, Phagocytosis, Phospholipids, Sialic Acids, Complement Factor H

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review