Evidence map›Paper›PMID 25973757›Full record

ArticleGenes and immunity

Suppression of autoimmunity by CD5(+) IL-10-producing B cells in lupus-prone mice.

Y Baglaenko, K P Manion, N-H Chang, C Loh, G Lajoie, J E Wither

Abstract read
PubMed Publisher
In one paragraph

Article in Genes and immunity. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. CD5-Positive Primary Cutaneous Diffuse Large B-Cell Lymphoma-Leg Type.Case reports in dermatological medicine · 2019
    Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. 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

6 authors.

Y Baglaenko1] Arthritis Center of Excellence, Department of Genetics and Development, Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada [2] Department of Immunology, University of Toronto, Toronto, Ontario, Canada.
K P Manion1] Arthritis Center of Excellence, Department of Genetics and Development, Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada [2] Department of Immunology, University of Toronto, Toronto, Ontario, Canada.
N-H ChangArthritis Center of Excellence, Department of Genetics and Development, Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada.
C Loh1] Arthritis Center of Excellence, Department of Genetics and Development, Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada [2] Department of Immunology, University of Toronto, Toronto, Ontario, Canada.
G Lajoie1] Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada [2] Department of Pathology, Mount Sinai Hospital, Toronto, Ontario, Canada [3] Department of Pathology, William Osler Health System, Brampton, Ontario, Canada.
J E Wither1] Arthritis Center of Excellence, Department of Genetics and Development, Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada [2] Department of Immunology, University of Toronto, Toronto, Ontario, Canada [3] Department of Medicine, University of Toronto, Toronto, Ontario, Canada.

Funding

Canadian Institutes of Health Research FRN 102551
6 · The paper itself

Abstract

Systemic lupus erythematosus is a complex autoimmune disorder characterized by the production of pathogenic anti-nuclear antibodies. Previous work from our laboratory has shown that the introgression of a New Zealand Black-derived chromosome 4 interval onto a lupus-prone background suppresses the disease. Interestingly, the same genetic interval promoted the expansion of both Natural Killer T- and CD5(+) B cells in suppressed mice. In this study, we show that ablation of NKT cells with a CD1d knockout had no impact on either the suppression of lupus or the expansion of CD5(+) B cells. On the other hand, suppressed mice had an expanded population of IL-10-producing B cells that predominantly localized to the CD5(+)CD1d(low) compartment. The expansion of CD5(+) B cells negatively correlated with the frequency of pro-inflammatory IL-17 A-producing T-cells and kidney damage. Adoptive transfer with a single injection of total B cells with an enriched CD5(+) compartment reduced the frequency of memory/activated, IFNγ-producing, and IL-17 A-producing CD4 T-cells but did not significantly reduce autoantibody levels. Taken together, these data suggest that the expansion of CD5(+) IL-10-producing B cells and not NKT cells protects against lupus in these mice, by limiting the expansion of pro-inflammatory IL-17 A- and IFNγ-producing CD4 T-cells.

Indexed as

AutoimmunityAnimalsB-LymphocytesCD4-Positive T-LymphocytesCD5 AntigensImmunologic MemoryInterleukin-10Lupus Erythematosus, SystemicMiceMice, Inbred NZBCD5 AntigensInterleukin-10

Identifiers

PMID25973757

What OpenQuestion holds

Textmetadata
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.