Mechanism of biliary atresia caused by T follicular helper cells-induced immune injury.


Journal

BMC pediatrics
ISSN: 1471-2431
Titre abrégé: BMC Pediatr
Pays: England
ID NLM: 100967804

Informations de publication

Date de publication:
17 Oct 2024
Historique:
received: 18 09 2023
accepted: 14 10 2024
medline: 18 10 2024
pubmed: 18 10 2024
entrez: 17 10 2024
Statut: epublish

Résumé

Biliary atresia (BA) has diverse and unclear pathogenesis, which may be related to immune response in response to a foreign stimulus. T follicular helper (Tfh) cells have been found to play an important role in various immune diseases. To investigate the expression of Tfh cells in BA and non-BA cholestatic diseases in children. Transcriptome sequencing and Gene Ontology (GO) enrichment analysis were performed to investigate the differences in gene expression between the BA group and the non-BA cholestasis group. Study the distribution of Tfh cells in liver tissues of the BA and non-BA cholestatic groups through single sample gene set enrichment analysis (ssGSEA). Tfh cells (CD3 Transcriptome sequencing showed differences in gene expression between the BA group and the non-BA cholestasis group. A total of 808 genes were up-regulated and 405 genes were down-regulated in BA, suggesting that there might be a specific immune response in BA. GO enrichment analysis showed that BA group had augmented response to foreign stimulus and increased metabolic process compared to the non-BA cholestatic group. The relative proportion of immune cells was analyzed by ssGSEA method. The proportions of Tfh cells, activated B cells, CD4 Tfh cells share in immune cascade involvement in BA. Our work support immune pathogenesis of the in response to a stimulus that might be foreign in BA.

Sections du résumé

BACKGROUND BACKGROUND
Biliary atresia (BA) has diverse and unclear pathogenesis, which may be related to immune response in response to a foreign stimulus. T follicular helper (Tfh) cells have been found to play an important role in various immune diseases.
AIMS OBJECTIVE
To investigate the expression of Tfh cells in BA and non-BA cholestatic diseases in children.
METHODS METHODS
Transcriptome sequencing and Gene Ontology (GO) enrichment analysis were performed to investigate the differences in gene expression between the BA group and the non-BA cholestasis group. Study the distribution of Tfh cells in liver tissues of the BA and non-BA cholestatic groups through single sample gene set enrichment analysis (ssGSEA). Tfh cells (CD3
RESULTS RESULTS
Transcriptome sequencing showed differences in gene expression between the BA group and the non-BA cholestasis group. A total of 808 genes were up-regulated and 405 genes were down-regulated in BA, suggesting that there might be a specific immune response in BA. GO enrichment analysis showed that BA group had augmented response to foreign stimulus and increased metabolic process compared to the non-BA cholestatic group. The relative proportion of immune cells was analyzed by ssGSEA method. The proportions of Tfh cells, activated B cells, CD4
CONCLUSION CONCLUSIONS
Tfh cells share in immune cascade involvement in BA. Our work support immune pathogenesis of the in response to a stimulus that might be foreign in BA.

Identifiants

pubmed: 39420296
doi: 10.1186/s12887-024-05152-9
pii: 10.1186/s12887-024-05152-9
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

669

Subventions

Organisme : Health Commission of Shanxi Province
ID : 2022074

Informations de copyright

© 2024. The Author(s).

Références

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Auteurs

Ze Ji (Z)

Shanxi Provincial Children's Hospital, Taiyuan, China.
Department of Pediatrics, Shanxi Medical University, Taiyuan, China.

Xiaoxia Wu (X)

Shanxi Provincial Children's Hospital, Taiyuan, China.

Hongxia Ren (H)

Shanxi Provincial Children's Hospital, Taiyuan, China. renhongxia2022@163.com.

Jiexiong Feng (J)

Department of Pediatric Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. 2002tj0515@hust.edu.cn.

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