Evidence map›Paper›PMID 25249575›Full record

ArticleDiabetes2015

B-1a lymphocytes attenuate insulin resistance.

Lei Shen, Melissa Hui Yen Chng, Michael N Alonso, Robert Yuan, Daniel A Winer, Edgar G Engleman

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

  1. Type 2 Diabetes: How Much of an Autoimmune Disease?Frontiers in endocrinology · 2019
    Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. B cells in non-lymphoid tissues.Nature reviews. Immunology · 2025
    Review
  15. Article
  16. Review
  17. Tipping the Scale: Atheroprotective IgM-Producing B Cells in Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Review
  18. Review
  19. Review
  20. Article

9 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

6 authors at 3 institutions in 3 countries.

Lei ShenShanghai Institute of Immunology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Melissa Hui Yen ChngDepartment of Pathology, Stanford University School of Medicine, Stanford, CA.
Michael N AlonsoDepartment of Pathology, Stanford University School of Medicine, Stanford, CA.
Robert YuanDepartment of Pathology, Stanford University School of Medicine, Stanford, CA.
Daniel A WinerDivision of Cellular & Molecular Biology, Diabetes Research Group, Toronto General Research Institute (TGRI), University Health Network, Toronto, Ontario, Canada edengleman@stanford.edu dan.winer@uhn.ca.
Edgar G EnglemanDepartment of Pathology, Stanford University School of Medicine, Stanford, CA edengleman@stanford.edu dan.winer@uhn.ca.
Stanford University · USShanghai Jiao Tong University · CNUniversity Health Network · CA

Funding

Defining Adaptive Immune Mechanisms of Insulin ResistanceR01DK096038 · NIDDK · STANFORD UNIVERSITY · PI ENGLEMAN, EDGAR G. · 2012 to 2015
$1.5M
CIHR 119414NIDDK NIH HHS 1R01-DK-096038NIDDK NIH HHS R01 DK096038
6 · The paper itself

Abstract

Obesity-associated insulin resistance, a common precursor of type 2 diabetes, is characterized by chronic inflammation of tissues, including visceral adipose tissue (VAT). Here we show that B-1a cells, a subpopulation of B lymphocytes, are novel and important regulators of this process. B-1a cells are reduced in frequency in obese high-fat diet (HFD)-fed mice, and EGFP interleukin-10 (IL-10) reporter mice show marked reductions in anti-inflammatory IL-10 production by B cells in vivo during obesity. In VAT, B-1a cells are the dominant producers of B cell-derived IL-10, contributing nearly half of the expressed IL-10 in vivo. Adoptive transfer of B-1a cells into HFD-fed B cell-deficient mice rapidly improves insulin resistance and glucose tolerance through IL-10 and polyclonal IgM-dependent mechanisms, whereas transfer of B-2 cells worsens metabolic disease. Genetic knockdown of B cell-activating factor (BAFF) in HFD-fed mice or treatment with a B-2 cell-depleting, B-1a cell-sparing anti-BAFF antibody attenuates insulin resistance. These findings establish B-1a cells as a new class of immune regulators that maintain metabolic homeostasis and suggest manipulation of these cells as a potential therapy for insulin resistance.

Indexed as

AnimalsBlood GlucoseB-Lymphocyte SubsetsDietary FatsFemaleGene Expression RegulationGlucose IntoleranceHumansImmunoglobulin MInsulin ResistanceInterleukin-10MaleMiceMice, Inbred C57BLMiddle AgedObesityBlood GlucoseDietary FatsImmunoglobulin MInterleukin-10

Identifiers

PMID25249575
PMCPMC4303967
OpenAlexW2105987065

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.