Evidence map›Paper›PMID 27041637›Full record

ArticleCellular & molecular immunology2017

CD205-TLR9-IL-12 axis contributes to CpG-induced oversensitive liver injury in HBsAg transgenic mice by promoting the interaction of NKT cells with Kupffer cells.

Xin Hou, Xiaolei Hao, Meijuan Zheng, Congfei Xu, Jun Wang, Rongbin Zhou, Zhigang Tian

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular & molecular immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  6. Article
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  9. Review
  10. The role of natural killer T cells in liver transplantation.Frontiers in cell and developmental biology · 2023
    Review
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  12. Article
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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 3 institutions in 1 country.

Xin HouAnhui Provincial Laboratory of Microbiology and Parasitology, Department of Microbiology and Parasitology, Anhui Medical University, Hefei 230032, China.
Xiaolei HaoInstitute of Immunology and CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, China.
Meijuan ZhengDepartment of Clinical Laboratory, First Affiliated Hospital of Anhui Medical University, Hefei 230022, China.
Congfei XuInnovation Center for Cell Biology, Hefei National Laboratory for Physical Sciences at Microscale, Hefei 230027, China.
Jun WangInstitute of Immunology and CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, China.
Rongbin ZhouInstitute of Immunology and CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, China.
Zhigang TianInstitute of Immunology and CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, China.
Hefei National Center for Physical Sciences at Nanoscale · CNAnhui Medical University · CNUniversity of Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gut-derived bacterial products contribute to liver inflammation and injury during chronic hepatitis B virus infection; however, the underlying mechanisms remain obscure. In this study, hepatitis B surface antigen transgenic (HBs-Tg) mice and their wild-type (WT) control C57BL/6 mice were injected with CpG-oligodeoxynucleotides (ODNs) to mimic the translocation of gut microbial products into the systemic circulation. We found that, compared with the WT mice, the HBs-Tg mice were oversensitive to CpG-ODN-induced liver injury, which was dependent on natural killer T (NKT) cells. CpG-ODN injection enhanced the expression of Fas ligand (FasL) on NKT cells. In addition, hepatocytes from the HBs-Tg mice expressed higher levels of Fas than did those from the WT mice, which was further augmented by CpG-ODN. Interaction of Fas and FasL was involved in the cytotoxicity of NKT cells against hepatocytes in the HBs-Tg mice. Moreover, Kupffer cells in the HBs-Tg mice expressed higher levels of CD205 and produced greater amounts of interleukin (IL)-12 than did those in the WT mice. Finally, the depletion of Kupffer cells, neutralization of IL-12 or specific silencing of CD205 on Kupffer cells significantly inhibited CpG-ODN-induced liver injury and NKT activation in the HBs-Tg mice. Our data suggest that CD205-expressing Kupffer cells respond to CpG-ODNs and subsequently release IL-12 to promote NKT cell activation. Activated NKT cells induce liver damage through the Fas signaling pathway in HBs-Tg mice.

Indexed as

AnimalsAntigens, CDAntigens, ViralCell CommunicationChemical and Drug Induced Liver InjuryCytotoxicity, ImmunologicFas Ligand Proteinfas ReceptorHepatitis B virusHepatocytesHumansInterleukin-12Kupffer CellsLectins, C-TypeLymphocyte ActivationMiceAntigens, CDAntigens, ViralCPG-oligonucleotideDEC-205 receptorFas Ligand ProteinFasl protein, mousefas ReceptorInterleukin-12Lectins, C-TypeMinor Histocompatibility AntigensOligodeoxyribonucleotidesReceptors, Cell SurfaceRNA, Small InterferingTlr9 protein, mouseToll-Like Receptor 9

Identifiers

PMID27041637
PMCPMC5549602
OpenAlexW2338172918

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.