Evidence map›Paper›PMID 30704426›Full record

ArticleBMC pediatrics2019

Distribution of distinct subsets of circulating T follicular helper cells in Kawasaki disease.

Meng Xu, Yanfang Jiang, Jinghua Wang, Deying Liu, Shaofeng Wang, Huanfa Yi, Sirui Yang

Open access · goldAbstract read
In one paragraph

Article in BMC pediatrics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. T-cell and autoantibody profiling for primary immune regulatory disorders.The Journal of allergy and clinical immunology · 2025
    Article
  3. Review
  4. The CXCL10-CXCR3 axis plays an important role in Kawasaki disease.Clinical and experimental immunology · 2024
    Article
  5. Article
  6. Article
  7. Congenital Heart Disease: An Immunological Perspective.Frontiers in cardiovascular medicine · 2021
    Review
  8. Article
  9. Review
  10. Article
  11. 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

7 authors at 1 institution in 1 country.

Meng XuDepartment of Pediatric Rheumatology and Allergy, The First Hospital of Jilin University, Changchun, 130021, China.
Yanfang JiangGenetic Diagnosis Center, The First Hospital of Jilin University, Changchun, 130021, China.
Jinghua WangDepartment of Pediatric Rheumatology and Allergy, The First Hospital of Jilin University, Changchun, 130021, China.
Deying LiuDepartment of Pediatric Rheumatology and Allergy, The First Hospital of Jilin University, Changchun, 130021, China.
Shaofeng WangThe Bethune Institute of Epigenetic Medicine, The First Hospital of Jilin University, Changchun, 130021, China.
Huanfa YiCentral Laboratory of the Eastern Division, The First Hospital of Jilin University, Changchun, 130021, China.
Sirui YangDepartment of Pediatric Rheumatology and Allergy, The First Hospital of Jilin University, Changchun, 130021, China. sryang@jlu.edu.cn.ORCID 0000-0001-7984-3569
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKawasaki disease (KD) is an acute febrile vasculitis that primarily affects children. Previous studies have shown that both innate and adapt immune systems are involved in the immunopathogenesis of KD. The following study analyzes the distribution of the subsets of Circulating T follicular helper cells (cTfh cells) in KD patients with and without coronary artery lesions (CALs).

methodsTwenty KD patients and fifteen healthy sex- and age- matched children were enrolled. Patients were divided into two groups depending on CALs. Blood samples were collected respectively before and after intravenous immunoglobulin (IVIG) administration. Circulating Tfh cells were categorized into three subsets by flow cytometry including cTfh1 (CXCR3 + CCR6-), cTfh2 (CXCR3-CCX6-) and cTfh17 (CXCR3-CCR6+) cells in circulating CD3 + CD4 + CXCR5 + CD45RA- T cells. Cytometric bead arrays were used to analyze the level of IFN-γ, IL-4 and IL-17A.

resultsWe found that frequency of cTfh2 cells was significantly elevated in KD patients before IVIG administration with low expression of cTfh1 cells, where the ratio of cTfh2 + cTfh17/cTfh1 significantly increased. Levels of IFN-γ, IL-4 and IL-17A in KD were significantly higher compared to controls. Further analysis showed that cTfh1 cells were negatively correlated with serum CRP, whereas cTfh2 cells were positively correlated with serum CRP and ESR. Comparison of different groups showed that frequency of cTfh1 cells in CALs+ group were significantly lower compared to CALs- group. In contrast, cTfh2 cells in CALs+ group significantly increased. After IVIG administration, frequency of cTfh2 cells and the ratio significantly decreased while the frequency of cTfh1 cells significantly increased. Meanwhile, all levels of cytokines decreased.

conclusionsOur data demonstrated that cTfh1 and cTfh2 cells participate in the pathogenesis of KD, and that the two subsets might be associated with CALs.

Indexed as

Child, PreschoolFemaleHumansInfantMaleMucocutaneous Lymph Node SyndromeT-Lymphocytes, Helper-InducerCoronary artery lesionscTfh cellsKawasaki disease

Identifiers

PMID30704426
PMCPMC6357512
OpenAlexW2947237414

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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.