Evidence map›Paper›PMID 15314683›Full record

ReviewThe Journal of clinical investigation2004

The T cell cometh: interplay between adaptive immunity and cytokine networks in rheumatoid arthritis.

Gary S Firestein

Erratum issuedOpen access · bronzeAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

30 citing papers in PubMed, 92 citations in OpenAlex.

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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Gary S FiresteinDivision of Rheumatology, Allergy, and Immunology and Clinical Investigation Institute, University of California San Diego School of Medicine, 9500 Gilman Drive, San Diego, CA 92093-0656, USA. gfirestein@ucsd.edu
University of California San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The etiology of autoimmunity in humans remains poorly defined, and animal models provide a unique opportunity to study potential autoimmune mechanisms. A novel model of autoimmune inflammatory arthritis results from a point mutation in the zeta-associated-protein of 70 kDa (ZAP-70), which causes abnormal thymic T cell selection and survival of autoreactive clones. Although the resulting clinical and pathologic abnormalities are clearly T cell-dependent, macrophage and fibroblast cytokines such as IL-1 and TNF-alpha are required for full expression of the disease. The studies of Hata et al. raise the intriguing possibility that traditional proinflammatory cytokine networks represent common effector mechanisms in inflammatory joint diseases such as rheumatoid arthritis. Hence, effective therapeutic interventions can target either unique etiologic pathways related to adaptive immune responses or shared terminal mechanisms.

Indexed as

AutoimmunityAnimalsArthritis, RheumatoidCytokinesFibroblastsHumansInterleukin-1MacrophagesModels, ImmunologicalPoint MutationProtein-Tyrosine KinasesT-LymphocytesTumor Necrosis Factor-alphaCytokinesInterleukin-1Protein-Tyrosine KinasesTumor Necrosis Factor-alpha

Identifiers

PMID15314683
PMCPMC503778
OpenAlexW1993986909

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.