Evidence map›Paper›PMID 29367461›Full record

ArticleJCI insight2018

CD122 blockade restores immunological tolerance in autoimmune type 1 diabetes via multiple mechanisms.

Xiaomei Yuan, Yi Dong, Naoya Tsurushita, J Yun Tso, Wenxian Fu

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Vitiligo: Pathogenesis and New and Emerging Treatments.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. TCF-1 Is Required for CD4 T Cell Persistence Functions during AlloImmunity.International journal of molecular sciences · 2023
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Advances in the Study of CD8+ Regulatory T Cells.Critical reviews in immunology · 2019
    Review
  19. Article
  20. Article
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

5 authors at 2 institutions in 1 country.

Xiaomei YuanPediatric Diabetes Research Center, Department of Pediatrics, UCSD, La Jolla, California, USA.
Yi DongPediatric Diabetes Research Center, Department of Pediatrics, UCSD, La Jolla, California, USA.
Naoya TsurushitaJN Biosciences, Mountain View, California, USA.
J Yun TsoJN Biosciences, Mountain View, California, USA.
Wenxian FuPediatric Diabetes Research Center, Department of Pediatrics, UCSD, La Jolla, California, USA.
University of California San Diego · USJN Biosciences (United States) · US

Funding

Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Andrea L Hevener · 2003 to 2026
$40.4M
San Diego Clinical and Translational Research InstituteUL1TR000100 · NCATS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FIRESTEIN, GARY S · 2012 to 2015
$19.7M
NCATS NIH HHS UL1 TR000100NIDDK NIH HHS P30 DK063491
6 · The paper itself

Abstract

Signaling through IL-2/IL-15Rβ (CD122) is essential for the differentiation and function of T cells and NK cells. A mAb against CD122 has been implicated to suppress autoimmune type 1 diabetes (T1D) development in animal models. However, the mechanisms remain poorly understood. We find that in vivo administration of an anti-CD122 mAb (CD122 blockade) restores immune tolerance in nonobese diabetic (NOD) mice via multiple mechanisms. First, CD122 blockade selectively ablates pathogenic NK cells and memory phenotype CD8+ T cells from pancreatic islets. In contrast, islet CD4+Foxp3+ Tregs are only mildly affected. Second, CD122 blockade suppresses IFN-γ production in islet immune cells. Third, CD122 blockade inhibits the conversion of islet Th17 cells into diabetogenic Th1 cells. Furthermore, a combination of anti-CD122 mAb and Treg-trophic cytokines (IL-2 or IL-33) enhances the abundance and function of islet Tregs. In summary, these data provide crucial mechanistic insights into CD122 blockade-mediated immunoregulation and support therapeutic benefits of this combinational treatment in T1D.

Indexed as

AnimalsAntibodies, MonoclonalCD8-Positive T-LymphocytesDiabetes Mellitus, Type 1Disease Models, AnimalDrug Therapy, CombinationFemaleHybridomasImmune ToleranceImmunologic FactorsInterleukin-2Interleukin-2 Receptor beta SubunitInterleukin-33Islets of LangerhansKiller Cells, NaturalMiceAntibodies, MonoclonalIL2 protein, humanIl2rb protein, mouseIL33 protein, humanImmunologic FactorsInterleukin-2Interleukin-2 Receptor beta SubunitInterleukin-33Recombinant ProteinsAutoimmunityCytokinesDiabetesInflammationNK cells

Identifiers

PMID29367461
PMCPMC5821175
OpenAlexW2785309276

What OpenQuestion holds

Textmetadata
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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.