Evidence map›Paper›PMID 32214904›Full record

ArticleMediators of inflammation2020

Leptin Regulated ILC2 Cell through the PI3K/AKT Pathway in Allergic Rhinitis.

Qingxiang Zeng, Xi Luo, Yiquan Tang, Wenlong Liu, Renzhong Luo

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Adipokines: masterminds of metabolic inflammation.Nature reviews. Immunology · 2025
    Review
  4. Review
  5. Review
  6. Review
  7. Group 2 Innate Lymphoid Cells in Allergic Rhinitis.Journal of inflammation research · 2024
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Akt isoforms in the immune system.Frontiers in immunology · 2022
    Review
  16. Article
  17. Review
  18. Review
  19. 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 1 institution in 1 country.

Qingxiang ZengDepartment of Otolaryngology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-8213-4971
Xi LuoDepartment of Otolaryngology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-3176-7824
Yiquan TangDepartment of Otolaryngology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Wenlong LiuDepartment of Otolaryngology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0001-6653-2382
Renzhong LuoDepartment of Otolaryngology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0003-4829-643X
Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent studies suggest that leptin is involved in Th2 response in allergic rhinitis (AR). However, the effect of leptin on type II innate lymphoid cells (ILC2s) in AR is not well characterized.

methodsTwenty-six AR patients and 20 healthy controls were enrolled. Serum leptin levels were measured, and their correlation with ILC2 and type II cytokines were analyzed using enzyme-linked immunosorbent assay (ELISA) and flow cytometry. ILC2 differentiation and cytokine production stimulated by human recombinant leptin were analyzed by real-time polymerase chain reaction (PCR) and ELISA. AR mouse models were also established to verify the effect of leptin on ILC2 cell regulation.

resultsOur results showed that elevated serum leptin in AR patients was correlated with the percentage of ILC2 and the expression of type II cytokines. The recombinant leptin enhanced the expression of ILC2 cell transcription factors and type II cytokine through the PI3K/AKT pathway. The AR mice treated with leptin showed as stronger ILC2 inflammation and symptoms compared with control mice.

conclusionsOur data provide evidence that upregulation of leptin promotes ILC2 responses in AR and this process was achieved through the PI3K/AKT pathway.

Indexed as

AdolescentAdultAnimalsBlotting, WesternCytokinesEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryHumansLeptinMaleMice, Inbred BALB CMiddle AgedPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReal-Time Polymerase Chain ReactionCytokinesLeptinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID32214904
PMCPMC7081033
OpenAlexW3010185493

What OpenQuestion holds

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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.