Evidence map›Paper›PMID 20727163›Full record

ArticleBMC immunology2010

Recombinant human complement component C2 produced in a human cell line restores the classical complement pathway activity in-vitro: an alternative treatment for C2 deficiency diseases.

Paolo G V Martini, Lynette C Cook, Scott Alderucci, Angela W Norton, Dianna M Lundberg, Susan M Fish, Knut Langsetmo, Göran Jönsson, Christian Lood, Birgitta Gullstrand and 10 more

Open access · goldAbstract read
In one paragraph

Article in BMC immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.2field-weighted citation impact, top 41% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Complement deficiencies in systemic lupus erythematosus.Current allergy and asthma reports · 2014
    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

20 authors at 3 institutions in 2 countries.

Paolo G V MartiniDepartment of Protein Expression and Purification Research, Shire Human Genetic Therapies Inc, 700 Main Street, Cambridge, MA 02139, USA. pmartini@shire.com
Lynette C Cook
Scott Alderucci
Angela W Norton
Dianna M Lundberg
Susan M Fish
Knut Langsetmo
Göran Jönsson
Christian Lood
Birgitta Gullstrand
Kate J Zaleski
Nancy Savioli
Jason Lottherand
Charles Bedard
John Gill
Michael F Concino
Michael W Heartlein
Lennart Truedsson
Jan L Powell
Arthur O Tzianabos
Protein Express (United States) · USTakeda (United States) · USLund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundComplement C2 deficiency is the most common genetically determined complete complement deficiency and is associated with a number of diseases. Most prominent are the associations with recurrent serious infections in young children and the development of systemic lupus erythematosus (SLE) in adults. The links with these diseases reflect the important role complement C2 plays in both innate immunity and immune tolerance. Infusions with normal fresh frozen plasma for the treatment of associated disease have demonstrated therapeutic effects but so far protein replacement therapy has not been evaluated.

resultsHuman complement C2 was cloned and expressed in a mammalian cell line. The purity of recombinant human C2 (rhC2) was greater than 95% and it was characterized for stability and activity. It was sensitive to C1s cleavage and restored classical complement pathway activity in C2-deficient serum both in a complement activation ELISA and a hemolytic assay. Furthermore, rhC2 could increase C3 fragment deposition on the human pathogen Streptococcus pneumoniae in C2-deficient serum to levels equal to those with normal serum.

conclusionsTaken together these data suggest that recombinant human C2 can restore classical complement pathway activity and may serve as a potential therapeutic for recurring bacterial infections or SLE in C2-deficient patients.

Indexed as

AdultCell Line, TransformedChildComplement C1Complement C2Complement C3Complement Pathway, ClassicalHumansImmunologic Deficiency SyndromesLupus Erythematosus, SystemicProtein BindingRecombinant ProteinsRecurrenceStreptococcal InfectionsStreptococcus pneumoniaeComplement C1Complement C2Complement C3Recombinant Proteins

Identifiers

PMID20727163
PMCPMC2931460
OpenAlexW2111120896

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.