Evidence map›Paper›PMID 17917046›Full record

ReviewImmunologic research2007

Human autoimmune diseases are specific antigen-driven T-cell diseases: identification of the antigens.

Chris D Platsoucas, Emilia L Oleszak

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2007. 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
0.1field-weighted citation impact, top 47% 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, 10 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  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.

Chris D PlatsoucasDepartment of Microbiology and Immunology, Temple University School of Medicine, 3400 North Broad Street, Philadelphia, PA 19140, USA. Chris.Platsoucas@temple.edu
Emilia L Oleszak
Temple College · USTemple University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We are investigating the hypothesis that most human autoimmune diseases are specific antigen-driven T-cell diseases. T-cell clones responding to specific antigenic epitopes are responsible for the initiation and/or the propagation of these diseases. Similarly, specific antigen-driven T-cell responses are responsible for the rejection of organ allografts and the immune response to tumors. Activated T cells provide the "engine" for the chronic inflammation that is associated with autoimmune diseases, organ graft rejection and tumor immunity. The best way to identify whether specific antigen-driven T cell responses are involved in the initiation and/or propagation of these disorders is to investigate whether T cells that infiltrate relevant tissues from these diseases contain monoclonal or oligoclonal, that is to say clonally expanded, populations of T cells. Identification of the T-cell antigen receptor (TCR) transcripts employed by the clonally expanded T cells in these patients permits the identification of the specific antigens that elicit these T-cell responses. These antigens may be responsible for the pathogenesis of these diseases. We will summarize here certain of our findings in this area of research.

Indexed as

AntigensAutoimmune DiseasesCerebrospinal FluidHumansMolecular MimicryReceptors, Antigen, T-CellT-LymphocytesTranscription, GeneticAntigensReceptors, Antigen, T-Cell

Identifiers

PMID17917046
OpenAlexW2123155780

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.