Evidence map›Paper›PMID 22903670›Full record

ReviewAdvances in experimental medicine and biology2012

Immunoregulation by naturally occurring and disease-associated autoantibodies : binding to cytokines and their role in regulation of T-cell responses.

Claus H Nielsen, Klaus Bendtzen

Open access · bronzeAbstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
4.6field-weighted citation impact, top 6% 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

6 citing papers in PubMed, 19 citations in OpenAlex.

  1. Observational
  2. Article
  3. Article
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  5. Review
  6. Article
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

2 authors at 2 institutions in 1 country.

Claus H NielsenInstitute for Inflammation Research, Department of Rheumatology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. claus.henrik.nielsen@rh.regionh.dk
Klaus Bendtzen
Copenhagen University Hospital · DKRigshospitalet · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of naturally occurring autoantibodies (NAbs) in homeostasis and in disease manifestations is poorly understood. In the present chapter, we review how NAbs may interfere with the cytokine network and how NAbs, through formation of complement-activating immune complexes with soluble self-antigens, may promote the uptake and presentation of self-molecules by antigen-presenting cells. Both naturally occurring and disease-associated autoantibodies against a variety of cytokines have been reported, including NAbs against interleukin (IL)-1α, IL-6, IL-8, IL-10, granulocyte-macrophage colony-stimulating factor, interferon (IFN)-α, IFN-β, IFN-γ, macrophage chemotactic protein-1 and IL-21. NAbs against a variety of other self-antigens have also been reported, and using thyroglobulin as an example we discuss how NAbs are capable of promoting uptake of immune complexes via complement receptors and Fc-receptors on antigen-presenting cells and thereby regulate T-cell activity. Knowledge of the influence of NAbs against cytokines on immune homeostasis is likely to have wide-ranging implications both in understanding pathogenesis and in treatment of many immunoinflammatory disorders, including a number of autoimmune and autoinflammatory diseases.

Indexed as

Antigen-Presenting CellsAutoantibodiesAutoantigensAutoimmune DiseasesCommunicable DiseasesComplement ActivationComplement System ProteinsCytokinesHumansInflammationProtein BindingReceptors, ComplementReceptors, FcThyroglobulinT-LymphocytesAutoantibodiesAutoantigensComplement System ProteinsCytokinesReceptors, ComplementReceptors, FcThyroglobulin

Identifiers

PMID22903670
PMCPMC7123141
OpenAlexW1543611788

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.