Evidence map›Paper›PMID 26314831›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2016

Selective Loss of Signaling Lymphocytic Activation Molecule Family Member 4-Positive CD8+ T Cells Contributes to the Decreased Cytotoxic Cell Activity in Systemic Lupus Erythematosus.

Katalin Kis-Toth, Denis Comte, Maria P Karampetsou, Vasileios C Kyttaris, Lakshmi Kannan, Cox Terhorst, George C Tsokos

Open access · greenAbstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

42 citing papers in PubMed, 60 citations in OpenAlex.

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  11. CD8International journal of molecular sciences · 2022
    Review
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  17. COVID-19 in patients with systemic lupus erythematosus: lessons learned from the inflammatory disease.Translational research : the journal of laboratory and clinical medicine · 2021
    Review
  18. Article
  19. SARS-CoV-2 vaccines in patients with SLE.Lupus science & medicine · 2021
    Article
  20. Review
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

7 authors at 2 institutions in 1 country.

Katalin Kis-TothBeth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Denis ComteBeth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Maria P KarampetsouBeth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Vasileios C KyttarisBeth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Lakshmi KannanBeth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Cox TerhorstBeth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
George C TsokosBeth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Beth Israel Deaconess Medical Center · USHarvard University · 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
NIAID NIH HHS 2P01-AI-065687-06A1NIAID NIH HHS P01 AI065687
6 · The paper itself

Abstract

objectiveEngagement of signaling lymphocytic activation molecule family member 4 (SLAMF4; CD244, 2B4) by its ligand SLAMF2 (CD48) modulates the function and expansion of both natural killer cells and a subset of cytotoxic CD8+ T cells. Because the cytotoxicity of CD8+ T lymphocytes isolated from patients with systemic lupus erythematosus (SLE) is known to be impaired, the aim of this study was to assess whether the expression and function of the checkpoint regulator SLAMF4 are altered on CD8+ T cells from patients with SLE.

methodsThe expression of SLAMF4 by T cells from healthy donors and patients with SLE was determined by quantitative polymerase chain reaction and flow cytometry. T cells were activated with anti-CD3 antibody, and degranulation activity was monitored by the surface expression of lysosome-associated membrane protein 1 (LAMP-1; CD107a). The SLAMF4+ and SLAMF4- CD8+ T cell subpopulations were characterized by LAMP-1, perforin, and granzyme B expression and viral peptide-induced proliferation.

resultsSLAMF4 gene and surface protein expression was down-regulated in CD8+ T cells from SLE patients compared with that in cells obtained from healthy donors. Importantly, SLE patients had significantly fewer SLAMF4+ CD8+ T cells compared with healthy donors. SLAMF4- CD8+ T cells from SLE patients had a decreased cytotoxic capacity and decreased proliferative responses to viral peptides. The loss of memory SLAMF4+ CD8+ T cells in SLE patients was linked to the fact that these cells have an increased propensity to lose CD8 expression and become double-negative T cells.

conclusionA selective loss of SLAMF4+ CD8+ T cells contributes to the compromised ability of T cells from patients with SLE to fight infection.

Indexed as

Antigens, CDBlotting, WesternCase-Control StudiesCD48 AntigenCD8-Positive T-LymphocytesCell ProliferationFlow CytometryGene ExpressionGranzymesHumansKiller Cells, NaturalLupus Erythematosus, SystemicLymphocyte ActivationPerforinReal-Time Polymerase Chain ReactionReceptors, ImmunologicAntigens, CDCD244 protein, humanCD48 AntigenCD48 protein, humanGranzymesPerforinReceptors, ImmunologicRNA, MessengerSignaling Lymphocytic Activation Molecule FamilyViral Proteins

Identifiers

PMID26314831
PMCPMC4690788
OpenAlexW2263880892

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.