Evidence map›Paper›PMID 20693344›Full record

ArticleDiabetes2010

Neutralization of interleukin-16 protects nonobese diabetic mice from autoimmune type 1 diabetes by a CCL4-dependent mechanism.

Craig Meagher, Josh Beilke, Guillermo Arreaza, Qing-Sheng Mi, Wei Chen, Konstantin Salojin, Noah Horst, William W Cruikshank, Terry L Delovitch

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. Trial
  2. Association ofBioscience reports · 2019
    Trial
  3. Review
  4. Emerging microbes & infections · 2024
    Article
  5. Article
  6. [Expression and clinical significance of interleukin-16 in patients with primary biliary cholangitis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Interleukin-16-producing NK cells and T-cells in the blood of tobacco smokers with and without COPD.International journal of chronic obstructive pulmonary disease · 2016
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Craig MeagherDepartment of Microbiology and Immunology, University of Western Ontario, London, Ontario, Canada.
Josh Beilke
Guillermo Arreaza
Qing-Sheng Mi
Wei Chen
Konstantin Salojin
Noah Horst
William W Cruikshank
Terry L Delovitch
Robarts Clinical Trials · CAUniversity of California, San Francisco · USBoston University · US

Funding

Canadian Institutes of Health Research MOP 64386
6 · The paper itself

Abstract

objectiveThe progressive infiltration of pancreatic islets by lymphocytes is mandatory for development of autoimmune type 1 diabetes. This inflammatory process is mediated by several mediators that are potential therapeutic targets to arrest development of type 1 diabetes. In this study, we investigate the role of one of these mediators, interleukin-16 (IL-16), in the pathogenesis of type 1 diabetes in NOD mice. RESEARCH DESIGN AND

methodsAt different stages of progression of type 1 diabetes, we characterized IL-16 in islets using GEArray technology and immunoblot analysis and also quantitated IL-16 activity in cell migration assays. IL-16 expression was localized in islets by immunofluorescence and confocal imaging. In vivo neutralization studies were performed to assess the role of IL-16 in the pathogenesis of type 1 diabetes.

resultsThe increased expression of IL-16 in islets correlated with the development of invasive insulitis. IL-16 immunoreactivity was found in islet infiltrating T-cells, B-cells, NK-cells, and dendritic cells, and within an insulitic lesion, IL-16 was derived from infiltrating cells. CD4(+) and CD8(+) T-cells as well as B220(+) B-cells were identified as sources of secreted IL-16. Blockade of IL-16 in vivo protected against type 1 diabetes by interfering with recruitment of CD4(+) T-cells to the pancreas, and this protection required the activity of the chemokine CCL4.

conclusionsIL-16 production by leukocytes in islets augments the severity of insulitis during the onset of type 1 diabetes. IL-16 and CCL4 appear to function as counterregulatory proteins during disease development. Neutralization of IL-16 may represent a novel therapy for the prevention of type 1 diabetes.

Indexed as

Adoptive TransferAnimalsCarbon TetrachlorideCD4-Positive T-LymphocytesCell MovementDiabetes Mellitus, Type 1HyperinsulinismImmunoblottingInterleukin-16Islets of LangerhansMiceMice, Inbred NODMice, SCIDPancreasRNA, MessengerT-LymphocytesCarbon TetrachlorideInterleukin-16RNA, Messenger

Identifiers

PMID20693344
PMCPMC2963545
OpenAlexW2117012825

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.