Evidence map›Paper›PMID 26365016›Full record

ArticleImmunology and cell biology2016

Hepatitis B virus X protein modulates renal tubular epithelial cell-induced T-cell and macrophage responses.

Xuan Wang, Ling Wang, Nan Zhu, Yi Zhou, Li-Jie Gu, Wei-Jie Yuan

Abstract read
PubMed Publisher
In one paragraph

Article in Immunology and cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.4field-weighted citation impact, top 31% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. HBx-induced PLARenal failure · 2023
    Article
  7. The Role of HBx Protein in Diseases Beyond the Liver.Infection and drug resistance · 2023
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. 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 2 institutions in 2 countries.

Xuan WangDepartment of Nephrology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ling WangDepartment of Nephrology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Nan ZhuDepartment of Nephrology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yi ZhouDepartment of Nephrology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Li-Jie GuDepartment of Nephrology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wei-Jie YuanDepartment of Nephrology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shanghai First People's Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal tubular epithelial cells (RTECs) have an active role in renal inflammation, functioning as antigen-presenting cells as they constitutively express major histocompatibility complex-II and co-stimulatory molecules that can activate T cells and macrophages. Previous studies indicate that inflammatory cell infiltration and tubulointerstitial fibrosis are present in renal biopsies from Hepatitis B virus (HBV)-associated glomerulonephritis (HBV-GN) patients. We hypothesized that disorder RTECs may be involved in the progression of HBV-GN. Here, we measured renal function and inflammatory cells infiltration in C57BL/6J-TgN mice, and data showed that in C57BL/6J-TgN mice HBV x protein (HBx) mainly deposited in RTECs, and CD4(+) T cells and macrophages infiltrated into the interstitium. In vitro HBx upregulated CD40 expression in RTECs. In HK-2/CD4(+) T cells co-culture system, we found that HBx-stimulated HK-2 cells could activate CD4(+) T cells, promote their proliferation, and lead to an imbalance of interleukin (IL)-4 and interferon-γ. In HK-2/macrophages co-culture system, we found that HBx-stimulated HK-2 cells also increased macrophage adherent capacity and promoted MCP-1 and tumor necrosis factor-α and IL-1β secretion. These immune dysfunction may contribute to the pathogenesis of HBV-GN.

Indexed as

AnimalsBiomarkersCD40 AntigensCell AdhesionCell LineCoculture TechniquesCytokinesEpithelial CellsFemaleGene ExpressionHumansImmunohistochemistryKidneyKidney Function TestsKidney TubulesLymphocyte ActivationBiomarkersCD40 AntigensCytokineshepatitis B virus X proteinTrans-ActivatorsViral Regulatory and Accessory Proteins

Identifiers

PMID26365016
OpenAlexW2238813453

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.