Evidence map›Paper›PMID 27545302›Full record

ArticleScientific reports2016

IL-21/IL-21R signaling suppresses intestinal inflammation induced by DSS through regulation of Th responses in lamina propria in mice.

Yuanyuan Wang, Xuefeng Jiang, Junfeng Zhu, Dan Yue, Xiaoqing Zhang, Xiao Wang, Yong You, Biao Wang, Ying Xu, Changlong Lu and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

27 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. CD126Orphanet journal of rare diseases · 2025
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. IL-21/IL-21R Promotes the Pro-Inflammatory Effects of Macrophages duringInternational journal of molecular sciences · 2023
    Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Frontiers in immunology · 2021
    Article
  20. 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

12 authors at 5 institutions in 2 countries.

Yuanyuan WangDepartment of anesthesiology, The Fourth Affiliated Hospital, China Medical University, Shenyang, China.
Xuefeng JiangDepartment of Immunology, China Medical University, Shenyang, China.
Junfeng ZhuLife Science School, Liaoning University, Shenyang, China.
Dan YueDepartment of Immunology, China Medical University, Shenyang, China.
Xiaoqing ZhangDepartment of Immunology, China Medical University, Shenyang, China.
Xiao WangDepartment of Immunology, China Medical University, Shenyang, China.
Yong YouDepartment of Immunology, China Medical University, Shenyang, China.
Biao WangDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences of China Medical University, Shenyang, China.
Ying XuNortheast Pharmaceutical Group Co., Ltd, Shenyang, China.
Changlong LuDepartment of Immunology, China Medical University, Shenyang, China.
Xun SunDepartment of Immunology, China Medical University, Shenyang, China.
Yasunobu YoshikaiDivision of Host Defense, Center for Prevention of Infectious Disease, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
China Medical University · CNFourth Affiliated Hospital of China Medical University · CNKyushu University · JPLiaoning University · CNSheng Jing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Serum level of IL-21 is increased in patients with inflammatory bowel diseases (IBD), suggesting that IL-21/IL-21 receptor (IL-21R) signaling may be involved in the pathogenesis of IBD. However, the role of IL-21/IL-21 receptor signaling plays in the pathogenesis of IBD is not very clear. In this study, using IL-21R.KO mice, we tested the role of IL-21/IL-21R signaling in the regulation of T helper cell responses during intestinal inflammation. Here we found that IL-21R.KO mice were more susceptible to DSS-induced colitis as compared with C57BL/6 mice. The spontaneous inflammatory cytokines released by macrophages in LP of colon were significantly increased, and Th2, Th17 and Treg responses were down-regulated markedly. However, Th1 responses were significantly up-regulated in IL-21R.KO mice. Meanwhile, the population of CD8(+)CD44(+)IFN-γ(+) T cells was markedly elevated in LP of inflammatory intestine of IL-21RKO mice. In vivo, after disease onset, DSS-induced intestinal inflammation was ameliorated in C57BL/6 mice treated with rIL-21. Our results demonstrate that IL-21/IL-21R signaling contributes to protection against DSS-induced acute colitis through suppression of Th1 and activation of Th2, Th17 and Treg responses in mice. Therefore, therapeutic manipulation of IL-21/IL-21R activity may allow improved immunotherapy for IBD and other inflammatory diseases associated with Th cell responses.

Indexed as

Signal TransductionAnimalsColitisDextran SulfateDisease Models, AnimalInterleukin-21 Receptor alpha SubunitInterleukin-22InterleukinsMiceMice, Inbred C57BLMice, KnockoutMucous MembraneTh17 CellsTh2 CellsT-Lymphocytes, RegulatoryDextran SulfateIl21r protein, mouseInterleukin-21 Receptor alpha SubunitInterleukin-22Interleukins

Identifiers

PMID27545302
PMCPMC4992961
OpenAlexW2516425563

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.