Evidence map›Paper›PMID 26608922›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

The Group B Streptococcus-Secreted Protein CIP Interacts with C4, Preventing C3b Deposition via the Lectin and Classical Complement Pathways.

Giampiero Pietrocola, Simonetta Rindi, Roberto Rosini, Scilla Buccato, Pietro Speziale, Immaculada Margarit

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Mucosal Vaccination withVaccines · 2020
    Article
  6. The Streptococcus agalactiae complement interfering protein combines multiple complement-inhibitory mechanisms by interacting with both C4 and C3 ligands.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  7. Article
  8. Review
  9. Frontiers in immunology · 2018
    Article
  10. Frontiers in immunology · 2018
    Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Novel Evasion Mechanisms of the Classical Complement Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2016
    Review
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

6 authors at 2 institutions in 2 countries.

Giampiero PietrocolaDepartment of Molecular Medicine, Unit of Biochemistry, University of Pavia, 27100 Pavia, Italy; and.ORCID http://orcid.org/0000-0002-7069-8155
Simonetta RindiDepartment of Molecular Medicine, Unit of Biochemistry, University of Pavia, 27100 Pavia, Italy; and.
Roberto RosiniGSK Vaccines S.r.l., 53100 Siena, Italy.
Scilla BuccatoGSK Vaccines S.r.l., 53100 Siena, Italy.
Pietro SpezialeDepartment of Molecular Medicine, Unit of Biochemistry, University of Pavia, 27100 Pavia, Italy; and immaculada.x.margarit-y-ros@gsk.com pspeziale@unipv.it.
Immaculada MargaritGSK Vaccines S.r.l., 53100 Siena, Italy immaculada.x.margarit-y-ros@gsk.com pspeziale@unipv.it.
GlaxoSmithKline (India) · INUniversity of Pavia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The group B Streptococcus (GBS) is a leading cause of neonatal invasive disease. GBS bacteria are surrounded by a thick capsular polysaccharide that is a potent inhibitor of complement deposition via the alternative pathway. Several of its surface molecules can however activate the classical and lectin complement pathways, rendering this species still vulnerable to phagocytic killing. In this study we have identified a novel secreted protein named complement interfering protein (CIP) that downregulates complement activation via the classical and lectin pathways, but not the alternative pathway. The CIP protein showed high affinity toward C4b and inhibited its interaction with C2, presumably preventing the formation of the C4bC2a convertase. Addition of recombinant CIP to GBS cip-negative bacteria resulted in decreased deposition of C3b on their surface and in diminished phagocytic killing in a whole-blood assay. Our data reveal a novel strategy exploited by GBS to counteract innate immunity and could be valuable for the development of anti-infective agents against this important pathogen.

Indexed as

AdultAmino Acid SequenceBacterial ProteinsComplement ActivationComplement C3bComplement C4bComplement Pathway, AlternativeComplement Pathway, ClassicalComplement Pathway, Mannose-Binding LectinHumansImmune EvasionImmunity, InnateMolecular Sequence DataPhagocytosisProtein BindingRecombinant ProteinsBacterial ProteinsComplement C3bComplement C4bRecombinant Proteins

Identifiers

PMID26608922
PMCPMC4683360
OpenAlexW2179582878

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.