Evidence map›Paper›PMID 26964093›Full record

ArticlePloS one2016

IL-10 Production Is Critical for Sustaining the Expansion of CD5+ B and NKT Cells and Restraining Autoantibody Production in Congenic Lupus-Prone Mice.

Yuriy Baglaenko, Kieran P Manion, Nan-Hua Chang, Eric Gracey, Christina Loh, Joan E Wither

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Frontiers in immunology · 2025
    Article
  3. Review
  4. Modulation of the Itaconate Pathway Attenuates Murine Lupus.Arthritis & rheumatology (Hoboken, N.J.) · 2022
    Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
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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

6 authors at 3 institutions in 1 country.

Yuriy BaglaenkoDepartment of Genetics and Development, Krembil Research Institute, University Health Network, Toronto, Ontario, Canada.
Kieran P ManionDepartment of Genetics and Development, Krembil Research Institute, University Health Network, Toronto, Ontario, Canada.
Nan-Hua ChangDepartment of Genetics and Development, Krembil Research Institute, University Health Network, Toronto, Ontario, Canada.
Eric GraceyDepartment of Genetics and Development, Krembil Research Institute, University Health Network, Toronto, Ontario, Canada.
Christina LohDepartment of Genetics and Development, Krembil Research Institute, University Health Network, Toronto, Ontario, Canada.
Joan E WitherDepartment of Genetics and Development, Krembil Research Institute, University Health Network, Toronto, Ontario, Canada.
University Health Network · CAKrembil Research InstituteUniversity of Toronto · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

The development and progression of systemic lupus erythematosus is mediated by the complex interaction of genetic and environmental factors. To decipher the genetics that contribute to pathogenesis and the production of pathogenic autoantibodies, our lab has focused on the generation of congenic lupus-prone mice derived from the New Zealand Black (NZB) strain. Previous work has shown that an NZB-derived chromosome 4 interval spanning 32 to 151 Mb led to expansion of CD5+ B and Natural Killer T (NKT) cells, and could suppress autoimmunity when crossed with a lupus-prone mouse strain. Subsequently, it was shown that CD5+ B cells but not NKT cells derived from these mice could suppress the development of pro-inflammatory T cells. In this paper, we aimed to further resolve the genetics that leads to expansion of these two innate-like populations through the creation of additional sub-congenic mice and to characterize the role of IL-10 in the suppression of autoimmunity through the generation of IL-10 knockout mice. We show that expansion of CD5+ B cells and NKT cells localizes to a chromosome 4 interval spanning 91 to 123 Mb, which is distinct from the region that mediates the majority of the suppressive phenotype. We also demonstrate that IL-10 is critical to restraining autoantibody production and surprisingly plays a vital role in supporting the expansion of innate-like populations.

Indexed as

CD5 AntigensInterleukin-10Lupus Erythematosus, SystemicAnimalsAutoantibodiesB-LymphocytesChromosomes, MammalianMice, Inbred NZBMice, KnockoutNatural Killer T-CellsAutoantibodiesCD5 AntigensCd5 protein, mouseIL10 protein, mouseInterleukin-10

Identifiers

PMID26964093
PMCPMC4786215
OpenAlexW2295690098

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.