Evidence map›Paper›PMID 25801878›Full record

ReviewLupus2015

T cells as a therapeutic target in SLE.

D Comte, M P Karampetsou, G C Tsokos

Abstract readReview
In one paragraph

Review in Lupus, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing 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

58 citing papers in PubMed.

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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.

D ComteDivision of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA Division of Immunology and Allergy, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland dcomte@bidmc.harvard.edu.
M P KarampetsouDivision of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
G C TsokosDivision of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.

Funding

The Slamf3, Slamf5, and Slamf6 receptor-induced pathways to murine lupusP01AI065687 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TERHORST, CORNELIS P · 2006 to 2016
$14.7M
LYMPHOCYTE SIGNALING DEFECTS IN PATIENTS WITH LUPUSR01AI042269 · NIAID · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI TSOKOS, GEORGE C · 1998 to 2017
$6.8M
Gene Transcription In SLER01AI049954 · NIAID · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI George C Tsokos · 2002 to 2026
$5.8M
NIAID NIH HHS AI065687NIAID NIH HHS P01 AI065687NIAID NIH HHS R01 AI042269NIAID NIH HHS R01 AI049954PHS HHS R01 42269
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease characterized by a loss of tolerance to multiple endogenous antigens. SLE etiology remains largely unknown, despite recent insight into the immunopathogenesis of the disease. T cells are important in the development of the disease by amplifying the immune response and contributing to organ damage. Aberrant signaling, cytokine secretion, and tissue homing displayed by SLE T cells have been extensively studied and the underlying pathogenic molecular mechanisms are starting to be elucidated. T-cell-targeted treatments are being explored in SLE patients. This review is an update on the T-cell abnormalities and related therapeutic options in SLE.

Indexed as

AnimalsCostimulatory and Inhibitory T-Cell ReceptorsEpigenesis, GeneticHumansImmune ToleranceInterleukin-2Lupus Erythematosus, SystemicSignal TransductionT-LymphocytesT-Lymphocyte SubsetsCostimulatory and Inhibitory T-Cell ReceptorsInterleukin-2epigeneticsinterleukin-2 (IL-2)Systemic lupus erythematosusT cellstreatment

Identifiers

PMID25801878
PMCPMC4372812

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.