Profiling of peripheral blood B-cell transcriptome in children who developed coeliac disease in a prospective study <sup>☆</sup>

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Abstract

Background

In coeliac disease (CoD), the role of B-cells has mainly been considered to be production of antibodies. The functional role of B-cells has not been analysed extensively in CoD.

Methods

We conducted a study to characterize gene expression in B-cells from children developing CoD early in life using samples collected before and at the diagnosis of the disease. Blood samples were collected from children at risk at 12, 18, 24 and 36 months of age. RNA from peripheral blood CD19 ⁺ cells was sequenced and differential gene expression was analysed using R package Limma.

Findings

Overall, we found one gene, HNRNPL, modestly downregulated in all patients (logFC −0·7; q = 0·09), and several others downregulated in those diagnosed with CoD already by the age of 2 years.

Interpretation

The data highlight the role of B-cells in CoD development. The role of HNRPL in suppressing enteroviral replication suggests that the predisposing factor for both CoD and enteroviral infections is the low level of HNRNPL expression.

Funding

EU FP7 grant no. 202063, EU Regional Developmental Fund and research grant PRG712, The Academy of Finland Centre of Excellence in Molecular Systems Immunology and Physiology Research (SyMMyS) 2012–2017, grant no. 250114) and, AoF Personalized Medicine Program (grant no. 292482), AoF grants 292335, 294337, 319280, 31444, 319280, 329277, 331790) and grants from the Sigrid Jusélius Foundation (SJF).

Related collections

Most cited references 49

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Analysis of the human tissue-specific expression by genome-wide integration of transcriptomics and antibody-based proteomics.

Linn Fagerberg, Björn Hallström, Per Oksvold … (2014)

Global classification of the human proteins with regards to spatial expression patterns across organs and tissues is important for studies of human biology and disease. Here, we used a quantitative transcriptomics analysis (RNA-Seq) to classify the tissue-specific expression of genes across a representative set of all major human organs and tissues and combined this analysis with antibody-based profiling of the same tissues. To present the data, we launch a new version of the Human Protein Atlas that integrates RNA and protein expression data corresponding to ∼80% of the human protein-coding genes with access to the primary data for both the RNA and the protein analysis on an individual gene level. We present a classification of all human protein-coding genes with regards to tissue-specificity and spatial expression pattern. The integrative human expression map can be used as a starting point to explore the molecular constituents of the human body.

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Gapped sequence alignment using artificial neural networks: application to the MHC class I system.

Massimo Andreatta, Morten A. Nielsen (2016)

Many biological processes are guided by receptor interactions with linear ligands of variable length. One such receptor is the MHC class I molecule. The length preferences vary depending on the MHC allele, but are generally limited to peptides of length 8-11 amino acids. On this relatively simple system, we developed a sequence alignment method based on artificial neural networks that allows insertions and deletions in the alignment.

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Multiple functions of p21 in cell cycle, apoptosis and transcriptional regulation after DNA damage.

Ansar Karimian, Seyyed Amir Yasin Ahmadi, Bahman Yousefi (2016)

An appropriate control over cell cycle progression depends on many factors. Cyclin-dependent kinase (CDK) inhibitor p21 (also known as p21(WAF1/Cip1)) is one of these factors that promote cell cycle arrest in response to a variety of stimuli. The inhibitory effect of P21 on cell cycle progression correlates with its nuclear localization. P21 can be induced by both p53-dependent and p53-independent mechanisms. Some other important functions attributed to p21 include transcriptional regulation, modulation or inhibition of apoptosis. These functions are largely dependent on direct p21/protein interactions and also on p21 subcellular localizations. In addition, p21 can play a role in DNA repair by interacting with proliferating cell nuclear antigen (PCNA). In this review, we will focus on the multiple functions of p21 in cell cycle regulation, apoptosis and gene transcription after DNA damage and briefly discuss the pathways and factors that have critical roles in p21 expression and activity.

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Author and article information

Contributors

Alar Aints

Journal

Journal ID (nlm-ta): Heliyon

Journal ID (iso-abbrev): Heliyon

Title: Heliyon

Publisher: Elsevier

ISSN (Electronic): 2405-8440

Publication date PMC-release: 21 January 2023

Publication date Collection: February 2023

Publication date (Electronic): 21 January 2023

Volume: 9

Issue: 2

Electronic Location Identifier: e13147

Affiliations

[a ]Department of Immunology, Institute of Biomedicine and Translational Medicine, University of Tartu, Estonia

[b ]Turku Bioscience Centre, University of Turku and Åbo Akademi University, Finland

[c ]InFLAMES Research Flagship Center, University of Turku, Turku, Finland

[d ]Institute of Biomedicine, University of Turku, Finland

[e ]Pediatric Research Center, Children's Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland

[f ]Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Helsinki, Finland

[g ]Center for Child Health Research, Tampere University Hospital, Tampere, Finland

Author notes

[∗ ]Corresponding author. Department of Immunology, Institute of Biomedicine and Translational Medicine, University of Tartu, Ravila 19, EE50411, Tartu, Estonia. Alar.Aints@ 123456ut.ee

Article

Publisher Item ID: S2405-8440(23)00354-7 Publisher ID: e13147

DOI: 10.1016/j.heliyon.2023.e13147

PMC ID: 9883278

PubMed ID: 36718152

SO-VID: ea446c7c-7c20-4060-9b9f-925104b4aa25

License:

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

History

Date received : 22 December 2021

Date revision received : 20 December 2022

Date accepted : 17 January 2023