Evidence map›Paper›PMID 25595787›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

Expansion of an atypical NK cell subset in mouse models of systemic lupus erythematosus.

Elisaveta N Voynova, Jeffrey Skinner, Silvia Bolland

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Natural killer cells in inflammatory autoimmune diseases.Clinical & translational immunology · 2021
    Review
  11. Article
  12. Dysregulation of TLR9 in neonates leads to fatal inflammatory disease driven by IFN-γ.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Non-pathogenic tissue-resident CD8Scientific reports · 2017
    Article
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 1 institution in 1 country.

Elisaveta N VoynovaLaboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville MD 20852.
Jeffrey SkinnerLaboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville MD 20852.
Silvia BollandLaboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville MD 20852 SBolland@niaid.nih.gov.
National Institute of Allergy and Infectious Diseases · US

Funding

Genetic Modifiers Of Autoimmune Disease In FcgammaRIIB Mutant MiceZIAAI000912 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI BOLLAND, SILVIA · 2009 to 2025
$27.0M
Intramural NIH HHS Z99 AI999999
6 · The paper itself

Abstract

Chronic inflammatory conditions, such as in autoimmune disease, can disturb immune cell homeostasis and induce the expansion of normally rare cell populations. In our analysis of various murine models of lupus, we detect increased frequency of an uncommon subset identified as NK1.1(+)CD11c(+)CD122(+)MHC class II(+). These cells share characteristics with the NK cell lineage and with cells previously described as IFN-producing killer dendritic cells: 1) they depend on IL-15 and express E4BP4; 2) they are cytotoxic and produce type I and type II IFN upon activation; and 3) they are efficient APCs both through MHC class II expression and in cross-presentation to CD8s. These atypical NK cells are responsive to TLR stimulation and thus are most abundant in mice with high copy number of the Tlr7 gene. They are highly proliferative as assessed by in vivo BrdU incorporation. In adoptive transfer experiments they persist in high numbers for months and maintain their surface marker profile, indicating that this population is developmentally stable. Gene expression analyses on both mRNA and microRNAs show a modified cell cycle program in which various miR-15/16 family members are upregulated, presumably as a consequence of the proliferative signal mediated by the increased level of growth factors, Ras and E2F activity. Alternatively, low expression of miR-150, miR-181, and miR-744 in these cells implies a reduction in their differentiation capacity. These results suggest that cells of the NK lineage that undergo TLR stimulation might turn on a proliferative program in detriment of their full differentiation into mature NK cells.

Indexed as

Adoptive TransferAnimalsCell DifferentiationCell LineageDisease Models, AnimalFemaleImmunohistochemistryKiller Cells, NaturalLupus Erythematosus, SystemicLymphocyte ActivationLymphocyte SubsetsMaleMiceMice, KnockoutMice, TransgenicMicroscopy, Electron, Transmission

Identifiers

PMID25595787
PMCPMC4323852
OpenAlexW2107446922

What OpenQuestion holds

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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.