Evidence map›Paper›PMID 15841173›Full record

ArticleThe Journal of clinical investigation2005

Altered regulation of IL-2 production in systemic lupus erythematosus: an evolving paradigm.

Gary M Kammer

Abstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2005. 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
1.0field-weighted citation impact, top 24% 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, 21 citations in OpenAlex.

  1. Review
  2. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Gary M KammerArthritis Associates Inc., Willoughby, Ohio 44094, USA. gmkammer@hotmail.com
Carolina Arthritis Associates · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In systemic lupus erythematosus (SLE), IL-2 production by T lymphocytes in vitro is impaired. Deficient IL-2 production may be an outcome of a primary SLE T cell disorder that is due to impaired signal transduction. In this issue of the JCI, evidence is presented that an anti-TCR/CD3 complex autoantibody present in SLE sera can bind to T cells and activate the Ca(2+)-calmodulin kinase IV (CaMKIV) signaling cascade, resulting in downregulation of IL-2 transcription and IL-2 production. Because IL-2 may contribute to the maintenance of T cell tolerance, deficient IL-2 production could promote a breach of T cell tolerance that results in autoantibody production in SLE.

Indexed as

AutoantibodiesCalcium-Calmodulin-Dependent Protein KinasesHumansImmune ToleranceInterleukin-2Lupus Erythematosus, SystemicReceptor-CD3 Complex, Antigen, T-CellSignal TransductionT-LymphocytesT-Lymphocyte SubsetsAutoantibodiesCalcium-Calmodulin-Dependent Protein KinasesInterleukin-2Receptor-CD3 Complex, Antigen, T-Cell

Identifiers

PMID15841173
PMCPMC1070433
OpenAlexW2142641379

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.