Evidence map›Paper›PMID 26554784›Full record

ArticleMedicine2015

The Distribution and the Fibrotic Role of Elevated Inflammatory Th17 Cells in Patients With Primary Biliary Cirrhosis.

TianYan Shi, Ting Zhang, LiNa Zhang, YunJiao Yang, HaoZe Zhang, FengChun Zhang

Open access · goldAbstract read
In one paragraph

Article in Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Bile acids and their receptors in hepatic immunity.Liver research (Beijing, China) · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. IL-21, not IL-17A, exacerbates murine primary biliary cholangitis.Clinical and experimental immunology · 2024
    Article
  7. Article
  8. Review
  9. Translational cancer research · 2023
    Article
  10. Article
  11. Article
  12. Review
  13. Intrahepatic TFrontiers in pharmacology · 2020
    Review
  14. Article
  15. Systemic effects of IL-17 in inflammatory arthritis.Nature reviews. Rheumatology · 2019
    Review
  16. Article
  17. Gal-3 Deficiency SuppressesFrontiers in immunology · 2019
    Article
  18. Article
  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

6 authors at 1 institution in 1 country.

TianYan ShiFrom the Department of Rheumatology and Clinical Immunology, Key Laboratory of Rheumatology & Clinical Immunology, Ministry of Education, Peking Union Medical College Hospital, Chinese Academy of Medical Science, Beijing, China.
Ting Zhang
LiNa Zhang
YunJiao Yang
HaoZe Zhang
FengChun Zhang
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T helper (Th) 17 cells were reported to have the property of proinflammation and profibrosis. We first investigate the levels of Th17 cells in primary biliary cirrhosis (PBC) patients, and then explore their distribution and fibrotic role in the disease.We compared the circulating Th17 and hepatic interleukin (IL)-17-positive cells between patients and healthy controls (HCs) at different disease stages by flow cytometry and immunohistochemistry, respectively. The levels of chemokine (c-c motif) ligand (CCL) 20 were then measured. For exploration of the reason why Th17 cells increased, CD4CD161 populations were sorted and cultured with IL-23 and IL-1β to analyze their proliferation and IL-17 secretions. The serum IL-23 and IL-1β were tested by enzyme-linked immunosorbent assay. The proliferation and expressions of α-smooth muscle actin and IL-8 of hepatic stellate cells (HSCs) were identified after stimulated by different concentrations of IL-17.Circulating and hepatic Th17 cells were elevated in PBC patients compared with HCs. Early PBC patients presented with more Th17 cells in periphery blood and less in the liver than advanced PBC patients. Accordingly, the levels of both serum and hepatic CCL20 for Th17 cells were higher, especially in those with advanced disease. The progenitor of Th17, CD4CD161 cell was increased in PBC. Moreover, the percentage of Th17 cells was positively related with CD4CD161 cell. After stimulation with IL-23 and IL-1β which were improved in PBC patients, CD4CD161 cells from PBC patients expressed more IL-17, although their proliferation were not different between 2 groups. IL-17 can promote the proliferation of HSCs at a dose-dependent method, and also increase the IL-8 expression in a dose/time-dependent way. Anti-IL-17 can neutralize the above reactions.CD4CD161 cells are a source of increased Th17 in PBC patients. With disease progression, Th17 population decreased in the circulation, accompanied by greater accumulation in the liver, which is regulated by CCL20 in advanced patients. IL-17 may be involved in the process of PBC fibrosis.

Indexed as

Immunity, CellularAdultCells, CulturedDisease ProgressionEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryHumansImmunohistochemistryInterleukin-17LiverLiver Cirrhosis, BiliaryMaleTh17 CellsIL17A protein, humanInterleukin-17

Identifiers

PMID26554784
PMCPMC4915885
OpenAlexW2191264975

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.