Evidence map›Paper›PMID 29868033›Full record

ReviewFrontiers in immunology2018

Aberrant T Cell Signaling and Subsets in Systemic Lupus Erythematosus.

Takayuki Katsuyama, George C Tsokos, Vaishali R Moulton

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed, 4 pooled it
18.4field-weighted citation impact, top 1% 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

128 citing papers in PubMed, 4 syntheses or guidelines pooled it, 214 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  7. Article
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  12. Review
  13. [Lupus erythematosus].Dermatologie (Heidelberg, Germany) · 2025
    Review
  14. Review
  15. Article
  16. Article
  17. Article
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  20. Article

68 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 1 country.

Takayuki KatsuyamaDivision of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States.
George C TsokosDivision of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States.
Vaishali R MoultonDivision of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States.
Harvard University · USBeth Israel Deaconess Medical Center · US

Funding

The Slamf3, Slamf5, and Slamf6 receptor-induced pathways to murine lupusP01AI065687 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI SHARPE, ARLENE H. · 2006 to 2016
$14.7M
Expanded Double Negative T cells in SLE.R01AI085567 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TSOKOS, GEORGE C · 2010 to 2025
$6.8M
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 SLER37AI049954 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TSOKOS, GEORGE C · 2013 to 2022
$4.8M
Role of splicing factor SRSF1 in T cell function and autoimmunityR01AR068974 · NIAMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ADAMOPOULOS, IANNIS ELIAS · 2016 to 2020
$2.2M
Targeting CaMK4 in SLER01AR064350 · NIAMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TSOKOS, GEORGE C · 2013 to 2017
$1.8M
NIAID NIH HHS P01 AI065687NIAID NIH HHS R01 AI042269NIAID NIH HHS R01 AI085567NIAID NIH HHS R37 AI049954NIAMS NIH HHS R01 AR064350NIAMS NIH HHS R01 AR068974
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a chronic multi-organ debilitating autoimmune disease, which mainly afflicts women in the reproductive years. A complex interaction of genetics, environmental factors and hormones result in the breakdown of immune tolerance to "self" leading to damage and destruction of multiple organs, such as the skin, joints, kidneys, heart and brain. Both innate and adaptive immune systems are critically involved in the misguided immune response against self-antigens. Dendritic cells, neutrophils, and innate lymphoid cells are important in initiating antigen presentation and propagating inflammation at lymphoid and peripheral tissue sites. Autoantibodies produced by B lymphocytes and immune complex deposition in vital organs contribute to tissue damage. T lymphocytes are increasingly being recognized as key contributors to disease pathogenesis. CD4 T follicular helper cells enable autoantibody production, inflammatory Th17 subsets promote inflammation, while defects in regulatory T cells lead to unchecked immune responses. A better understanding of the molecular defects including signaling events and gene regulation underlying the dysfunctional T cells in SLE is necessary to pave the path for better management, therapy, and perhaps prevention of this complex disease. In this review, we focus on the aberrations in T cell signaling in SLE and highlight therapeutic advances in this field.

Indexed as

Signal TransductionAnimalsAutoimmunityBiomarkersCytokinesGene Expression RegulationHumansHyaluronan ReceptorsLupus Erythematosus, SystemicMolecular Targeted TherapyPhosphatidylinositol 3-KinasesPTEN PhosphohydrolaseReceptors, Antigen, T-Cellrho-Associated KinasesT-Lymphocyte SubsetsTOR Serine-Threonine KinasesBiomarkersCytokinesHyaluronan ReceptorsPhosphatidylinositol 3-KinasesPTEN PhosphohydrolaseReceptors, Antigen, T-Cellrho-Associated KinasesTOR Serine-Threonine KinasesAutoimmune diseaseautoimmunitysignalingSLET cells

Identifiers

PMID29868033
PMCPMC5967272
OpenAlexW2799912959

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.