Evidence map›Paper›PMID 16738955›Full record

ReviewSpringer seminars in immunopathology2006

Biological therapies directed against cells in autoimmune disease.

Paul Hasler

Abstract readReview
PubMed Publisher
In one paragraph

Review in Springer seminars in immunopathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 27 citations in OpenAlex.

  1. Are biological agents toxic to human chondrocytes and osteocytes?Journal of orthopaedic surgery and research · 2015
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Protective role of gammadelta T cells in spontaneous ocular inflammation.Investigative ophthalmology & visual science · 2009
    Article
  7. Article
  8. Article
  9. Review
  10. 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

1 author at 1 institution in 1 country.

Paul HaslerRheumaklinik, Kantonsspital Aarau, Tellstrasse, 5001 Aarau, Switzerland. paul.hasler@ksa.ch
Kantonsspital Aarau · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Among the cells of the immune system involved in the pathogenesis of autoimmune disease, T cells have received the most attention. The central role of these cells in several animal models of autoimmune diseases and in human disease counterparts has provided the rationale for specific therapeutic targeting of T cell subsets, especially CD4 T cells. So far, the applicability of this approach has not been clearly evident in clinical trials, which was also the case when nondepleting "coating" anti-CD4 monoclonal antibodies was used. In the past several years, experimental evidence supporting a major role of B cells in systemic autoimmune disease has grown. This includes the pathogenicity of certain autoantibodies, the potential of B cells to present antigen in the context of MHC Class II and to signal via costimulatory molecules, and to secrete proinflammatory cytokines. In some instances, engagement of the B cell receptor and other surface receptors is sufficient to stimulate B cells to produce antibodies. The depletion of B cells by targeting the surface marker CD20 has been shown to be effective in treating rheumatoid arthritis with a good side effect profile. Series of cases with other systemic autoimmune diseases indicate that this strategy may be effective in these conditions too. The clinical data add weight to the importance of B cells in the pathogenesis of autoimmune diseases.

Indexed as

AnimalsArthritis, RheumatoidAutoimmune DiseasesB-LymphocytesHumansImmunologic FactorsImmunotherapyMiceRatsT-LymphocytesImmunologic Factors

Identifiers

PMID16738955
OpenAlexW2017711212

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.