Evidence map›Paper›PMID 22231516›Full record

ReviewClinical reviews in allergy & immunology2013

Type I interferons: beneficial in Th1 and detrimental in Th17 autoimmunity.

Robert C Axtell, Chander Raman, Lawrence Steinman

Abstract readReview
In one paragraph

Review in Clinical reviews in allergy & immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
–field-weighted citation impact
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

49 citing papers in PubMed.

  1. Review
  2. Article
  3. SHP2: its association and roles in systemic lupus erythematosus.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Observational
  12. Article
  13. Review
  14. The IL-27/IL-27R axis is altered in CD4Clinical & translational immunology · 2021
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

3 authors.

Robert C AxtellDepartment of Neurology and Neurological Sciences, Stanford University, Stanford, CA, USA. axterobe@stanford.edu
Chander Raman
Lawrence Steinman

Funding

TRAINING PROGRAM IN RHEUMATIC DISEASES RESEARCHT32AR007450 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BRIDGES, S LOUIS · 1986 to 2011
$2.2M
Molecular Stratification of Multiple Sclerosis and Associated Neuro-autoimmune DiK99NS075099 · NINDS · STANFORD UNIVERSITY · PI AXTELL, ROBERT C · 2011 to 2012
$179k
NINDS NIH HHS K99 NS075099
6 · The paper itself

Abstract

In relapsing remitting multiple sclerosis (RRMS), type I interferon (IFN) is considered immuno-modulatory, and recombinant forms of IFN-β are the most prescribed treatment for this disease. However, within the RRMS population, 30-50% of MS patients are nonresponsive to this treatment, and it consistently worsens neuromyelitis optica (NMO), a disease once considered to be a form of RRMS. In contrast to RRMS, type I IFNs have been shown to have properties that drive the inflammatory pathologies in many other autoimmune diseases. These diseases include Sjögren's syndrome, system lupus erythematosus (SLE), neuromyelitis optica (NMO), rheumatoid arthritis (RA) and psoriasis. Historically, autoimmune diseases were thought to be driven by a TH1 response to auto-antigens. However, since the discovery of the TH17 in experimental autoimmune encephalomyelitis (EAE), it is now generally thought that TH17 plays an important role in MS and all other autoimmune diseases. In this article, we will discuss recent clinical and basic research advances in the field of autoimmunity and argue that IFN-β and other type I IFNs are immuno-modulatory in diseases driven predominantly by TH1 but in contrast are inflammatory in diseases that have a predominant Th17 response.

Indexed as

ImmunomodulationAnimalsAutoantigensAutoimmune DiseasesAutoimmunityDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalHumansInterferon Type IMiceTh17 CellsTh1 CellsAutoantigensInterferon Type I

Identifiers

PMID22231516
PMCPMC5478162

What OpenQuestion holds

Textmetadata
LicenceTDM
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.