Evidence map›Paper›PMID 34622804›Full record

ArticleJCI insight2021

IL-35 promotes CD4+Foxp3+ Tregs and inhibits atherosclerosis via maintaining CCR5-amplified Treg-suppressive mechanisms.

Ying Shao, William Y Yang, Fatma Saaoud, Charles Drummer, Yu Sun, Keman Xu, Yifan Lu, Huimin Shan, Ethan M Shevach, Xiaohua Jiang and 2 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. The role and mechanism of IL‑35 in myasthenia gravis (Review).International journal of molecular medicine · 2026
    Review
  9. Article
  10. Cytokines Associated with Activation of CD4International journal of molecular sciences · 2026
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Pro-Resolving Macrophage-Induced IL-35International journal of molecular sciences · 2025
    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

12 authors at 3 institutions in 1 country.

Ying ShaoCenters for Cardiovascular Research.
William Y YangCenters for Cardiovascular Research.
Fatma SaaoudCenters for Cardiovascular Research.
Charles DrummerCenters for Cardiovascular Research.
Yu SunCenters for Cardiovascular Research.
Keman XuCenters for Cardiovascular Research.
Yifan LuCenters for Cardiovascular Research.
Huimin ShanMetabolic Disease Research & Thrombosis Research, Department of Cardiovascular Sciences, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, USA.
Ethan M ShevachLaboratory of Immune System Biology, Cellular Immunology Section, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland, USA.
Xiaohua JiangCenters for Cardiovascular Research.
Hong WangMetabolic Disease Research & Thrombosis Research, Department of Cardiovascular Sciences, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, USA.
Xiaofeng YangCenters for Cardiovascular Research.
The Centers · USTemple University · USNational Institute of Allergy and Infectious Diseases · US

Funding

CD40 monocyte in chronic kidney diseaseR01DK113775 · NIDDK · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2017 to 2021
$3.3M
Caspase-1 activation mediates chronic kidney disease-accelerated atherosclerosisR01HL131460 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI CHOI, ERIC T., WANG, HONG · 2016 to 2019
$2.8M
The roles of miR-155 in regulating atherosclerosis and metabolically healthy obesityR01HL138749 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2017 to 2020
$2.6M
IL-35 inhibits gut microbiota-produced uremic toxin-accelerated endothelial cell activationR01HL147565 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2019 to 2022
$2.6M
Atherogenic roles of complement systemR01HL130233 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI QIN, XUEBIN, WANG, HONG · 2016 to 2019
$2.5M
IL-35 suppression of endothelial cell activation and atherosclerosisR01HL132399 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAOFENG · 2017 to 2020
$2.3M
HHcy-induced Inflammatory Monocyte and Macrophage Differentiation in DiabetesR01DK104116 · NIDDK · TEMPLE UNIV OF THE COMMONWEALTH · PI WANG, HONG · 2015 to 2019
$2.2M
NHLBI NIH HHS R01 HL130233NHLBI NIH HHS R01 HL131460NHLBI NIH HHS R01 HL132399NHLBI NIH HHS R01 HL138749NHLBI NIH HHS R01 HL147565NIDDK NIH HHS R01 DK104116NIDDK NIH HHS R01 DK113775
6 · The paper itself

Abstract

Tregs play vital roles in suppressing atherogenesis. Pathological conditions reshape Tregs and increase Treg-weakening plasticity. It remains unclear how Tregs preserve their function and how Tregs switch into alternative phenotypes in the environment of atherosclerosis. In this study, we observed a great induction of CD4+Foxp3+ Tregs in the spleen and aorta of ApoE-/- mice, accompanied by a significant increase of plasma IL-35 levels. To determine if IL-35 devotes its role in the rise of Tregs, we generated IL-35 subunit P35-deficient (IL-35P35-deficient) mice on an ApoE-/- background and found Treg reduction in the spleen and aorta compared with ApoE-/- controls. In addition, our RNA sequencing data show the elevation of a set of chemokine receptor transcripts in the ApoE-/- Tregs, and we have validated higher CCR5 expression in ApoE-/- Tregs in the presence of IL-35 than in the absence of IL-35. Furthermore, we observed that CCR5+ Tregs in ApoE-/- have lower Treg-weakening AKT-mTOR signaling, higher expression of inhibitory checkpoint receptors TIGIT and PD-1, and higher expression of IL-10 compared with WT CCR5+ Tregs. In conclusion, IL-35 counteracts hyperlipidemia in maintaining Treg-suppressive function by increasing 3 CCR5-amplified mechanisms, including Treg migration, inhibition of Treg weakening AKT-mTOR signaling, and promotion of TIGIT and PD-1 signaling.

Indexed as

AnimalsAortaAtherosclerosisCD4-Positive T-LymphocytesCell MovementForkhead Transcription FactorsInterleukin-10InterleukinsMiceMice, KnockoutMice, Knockout, ApoEProgrammed Cell Death 1 ReceptorProto-Oncogene Proteins c-aktReceptors, CCR5Receptors, ImmunologicSignal TransductionCCR5 protein, mouseForkhead Transcription FactorsFoxp3 protein, mouseIL10 protein, mouseInterleukin-10interleukin-35, mouseInterleukinsPdcd1 protein, mouseProgrammed Cell Death 1 ReceptorProto-Oncogene Proteins c-aktReceptors, CCR5Receptors, ImmunologicT cell Ig and ITIM domain protein, mouseTOR Serine-Threonine KinasesAtherosclerosisCardiologyCellular immune responseCytokinesInflammation

Identifiers

PMID34622804
PMCPMC8525592
OpenAlexW3201902111

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.