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Article ; Online: Dissecting the dynamic transcriptional landscape of early T helper cell differentiation into Th1, Th2, and Th1/2 hybrid cells.

Burt, Philipp / Peine, Michael / Peine, Caroline / Borek, Zuzanna / Serve, Sebastian / Floßdorf, Michael / Hegazy, Ahmed N / Höfer, Thomas / Löhning, Max / Thurley, Kevin

Frontiers in immunology

2022 Volume 13, Page(s) 928018

Abstract: Selective differentiation of CD4+ T helper (Th) cells into specialized subsets such as Th1 and Th2 cells is a key element of the adaptive immune system driving appropriate immune responses. Besides those canonical Th-cell lineages, hybrid phenotypes such ...

Abstract	Selective differentiation of CD4+ T helper (Th) cells into specialized subsets such as Th1 and Th2 cells is a key element of the adaptive immune system driving appropriate immune responses. Besides those canonical Th-cell lineages, hybrid phenotypes such as Th1/2 cells arise
MeSH term(s)	Cell Differentiation/genetics ; Hybrid Cells ; Lymphocyte Activation ; Th1 Cells ; Th2 Cells
Language	English
Publishing date	2022-08-16
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.928018
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Article: Genetic variation in the non-coding genome: Involvement of micro-RNAs and long non-coding RNAs in disease.

Hrdlickova, Barbara / de Almeida, Rodrigo Coutinho / Borek, Zuzanna / Withoff, Sebo

Biochimica et biophysica acta

2014 Volume 1842, Issue 10, Page(s) 1910–1922

Abstract: It has been found that the majority of disease-associated genetic variants identified by genome-wide association studies are located outside of protein-coding regions, where they seem to affect regions that control transcription (promoters, enhancers) ... ...

Abstract	It has been found that the majority of disease-associated genetic variants identified by genome-wide association studies are located outside of protein-coding regions, where they seem to affect regions that control transcription (promoters, enhancers) and non-coding RNAs that also can influence gene expression. In this review, we focus on two classes of non-coding RNAs that are currently a major focus of interest: micro-RNAs and long non-coding RNAs. We describe their biogenesis, suggested mechanism of action, and discuss how these non-coding RNAs might be affected by disease-associated genetic alterations. The discovery of these alterations has already contributed to a better understanding of the etiopathology of human diseases and yielded insight into the function of these non-coding RNAs. We also provide an overview of available databases, bioinformatics tools, and high-throughput techniques that can be used to study the mechanism of action of individual non-coding RNAs. This article is part of a Special Issue entitled: From Genome to Function.
Language	English
Publishing date	2014-10
Publishing country	Netherlands
Document type	Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2014.03.011
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Article ; Online: Potential impact of celiac disease genetic risk factors on T cell receptor signaling in gluten-specific CD4+ T cells.

Bakker, Olivier B / Ramírez-Sánchez, Aarón D / Borek, Zuzanna A / de Klein, Niek / Li, Yang / Modderman, Rutger / Kooy-Winkelaar, Yvonne / Johannesen, Marie K / Matarese, Filomena / Martens, Joost H A / Kumar, Vinod / van Bergen, Jeroen / Qiao, Shuo-Wang / Lundin, Knut E A / Sollid, Ludvig M / Koning, Frits / Wijmenga, Cisca / Withoff, Sebo / Jonkers, Iris H

Scientific reports

2021 Volume 11, Issue 1, Page(s) 9252

Abstract: Celiac disease is an auto-immune disease in which an immune response to dietary gluten leads to inflammation and subsequent atrophy of small intestinal villi, causing severe bowel discomfort and malabsorption of nutrients. The major instigating factor ... ...

Abstract	Celiac disease is an auto-immune disease in which an immune response to dietary gluten leads to inflammation and subsequent atrophy of small intestinal villi, causing severe bowel discomfort and malabsorption of nutrients. The major instigating factor for the immune response in celiac disease is the activation of gluten-specific CD4+ T cells expressing T cell receptors that recognize gluten peptides presented in the context of HLA-DQ2 and DQ8. Here we provide an in-depth characterization of 28 gluten-specific T cell clones. We assess their transcriptional and epigenetic response to T cell receptor stimulation and link this to genetic factors associated with celiac disease. Gluten-specific T cells have a distinct transcriptional profile that mostly resembles that of Th1 cells but also express cytokines characteristic of other types of T-helper cells. This transcriptional response appears not to be regulated by changes in chromatin state, but rather by early upregulation of transcription factors and non-coding RNAs that likely orchestrate the subsequent activation of genes that play a role in immune pathways. Finally, integration of chromatin and transcription factor binding profiles suggest that genes activated by T cell receptor stimulation of gluten‑specific T cells may be impacted by genetic variation at several genetic loci associated with celiac disease.
MeSH term(s)	Biomarkers/metabolism ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; Celiac Disease/chemically induced ; Celiac Disease/genetics ; Celiac Disease/immunology ; Celiac Disease/pathology ; Cytokines/immunology ; Cytokines/metabolism ; Gene Expression Profiling ; Gene Expression Regulation ; Glutens/administration & dosage ; Glutens/immunology ; Humans ; Receptors, Antigen, T-Cell/genetics ; Receptors, Antigen, T-Cell/immunology ; Transcriptome
Chemical Substances	Biomarkers ; Cytokines ; Receptors, Antigen, T-Cell ; Glutens (8002-80-0)
Language	English
Publishing date	2021-04-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-86612-5
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Article: Systematic Prioritization of Candidate Genes in Disease Loci Identifies

Frontiers in genetics

2021 Volume 11, Page(s) 562434

Abstract: Celiac disease (CeD) is a complex T cell-mediated enteropathy induced by gluten. Although genome-wide association studies have identified numerous genomic regions associated with CeD, it is difficult to accurately pinpoint which genes in these loci are ... ...

Abstract	Celiac disease (CeD) is a complex T cell-mediated enteropathy induced by gluten. Although genome-wide association studies have identified numerous genomic regions associated with CeD, it is difficult to accurately pinpoint which genes in these loci are most likely to cause CeD. We used four different
Language	English
Publishing date	2021-01-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2020.562434
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Article ; Online: Systematic Prioritization of Candidate Genes in Disease Loci Identifies as a Master Regulator of IFNγ Signaling in Celiac Disease.

11 ; 562434 ; Frontiers in genetics ; Switzerland

2021

Abstract	Celiac disease (CeD) is a complex T cell-mediated enteropathy induced by gluten. Although genome-wide association studies have identified numerous genomic regions associated with CeD, it is difficult to accurately pinpoint which genes in these loci are most likely to cause CeD. We used four different in silico approaches-Mendelian randomization inverse variance weighting, COLOC, LD overlap, and DEPICT-to integrate information gathered from a large transcriptomics dataset. This identified 118 prioritized genes across 50 CeD-associated regions. Co-expression and pathway analysis of these genes indicated an association with adaptive and innate cytokine signaling and T cell activation pathways. Fifty-one of these genes are targets of known drug compounds or likely druggable genes, suggesting that our methods can be used to pinpoint potential therapeutic targets. In addition, we detected 172 gene combinations that were affected by our CeD-prioritized genes in trans. Notably, 41 of these trans-mediated genes appear to be under control of one master regulator, TRAF-type zinc finger domain containing 1 (TRAFD1), and were found to be involved in interferon (IFN)γ signaling and MHC I antigen processing/presentation. Finally, we performed in vitro experiments in a human monocytic cell line that validated the role of TRAFD1 as an immune regulator acting in trans. Our strategy confirmed the role of adaptive immunity in CeD and revealed a genetic link between CeD and IFNγ signaling as well as with MHC I antigen processing, both major players of immune activation and CeD pathogenesis.
Keywords	TRAFD1 ; celiac disease ; expression quantitative trait locus (eQTL) ; gene prioritization ; trans regulation
Subject code	570 ; 572
Language	English
Publishing date	2021-01-25
Publisher	Frontiers
Publishing country	de
Document type	Article ; Online
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Article ; Online: Deconvolution of bulk blood eQTL effects into immune cell subpopulations.

Aguirre-Gamboa, Raúl / de Klein, Niek / di Tommaso, Jennifer / Claringbould, Annique / van der Wijst, Monique Gp / de Vries, Dylan / Brugge, Harm / Oelen, Roy / Võsa, Urmo / Zorro, Maria M / Chu, Xiaojin / Bakker, Olivier B / Borek, Zuzanna / Ricaño-Ponce, Isis / Deelen, Patrick / Xu, Cheng-Jiang / Swertz, Morris / Jonkers, Iris / Withoff, Sebo /

Joosten, Irma / Sanna, Serena / Kumar, Vinod / Koenen, Hans J P M / Joosten, Leo A B / Netea, Mihai G / Wijmenga, Cisca / Franke, Lude / Li, Yang

BMC bioinformatics

2020 Volume 21, Issue 1, Page(s) 243

Abstract: Background: Expression quantitative trait loci (eQTL) studies are used to interpret the function of disease-associated genetic risk factors. To date, most eQTL analyses have been conducted in bulk tissues, such as whole blood and tissue biopsies, which ... ...

Abstract	Background: Expression quantitative trait loci (eQTL) studies are used to interpret the function of disease-associated genetic risk factors. To date, most eQTL analyses have been conducted in bulk tissues, such as whole blood and tissue biopsies, which are likely to mask the cell type-context of the eQTL regulatory effects. Although this context can be investigated by generating transcriptional profiles from purified cell subpopulations, current methods to do this are labor-intensive and expensive. We introduce a new method, Decon2, as a framework for estimating cell proportions using expression profiles from bulk blood samples (Decon-cell) followed by deconvolution of cell type eQTLs (Decon-eQTL). Results: The estimated cell proportions from Decon-cell agree with experimental measurements across cohorts (R ≥ 0.77). Using Decon-cell, we could predict the proportions of 34 circulating cell types for 3194 samples from a population-based cohort. Next, we identified 16,362 whole-blood eQTLs and deconvoluted cell type interaction (CTi) eQTLs using the predicted cell proportions from Decon-cell. CTi eQTLs show excellent allelic directional concordance with eQTL (≥ 96-100%) and chromatin mark QTL (≥87-92%) studies that used either purified cell subpopulations or single-cell RNA-seq, outperforming the conventional interaction effect. Conclusions: Decon2 provides a method to detect cell type interaction effects from bulk blood eQTLs that is useful for pinpointing the most relevant cell type for a given complex disease. Decon2 is available as an R package and Java application (https://github.com/molgenis/systemsgenetics/tree/master/Decon2) and as a web tool (www.molgenis.org/deconvolution).
MeSH term(s)	Genome-Wide Association Study/methods ; Humans ; Quantitative Trait Loci/immunology ; Whole-Body Counting/methods
Language	English
Publishing date	2020-06-12
Publishing country	England
Document type	Journal Article
ZDB-ID	2041484-5
ISSN	1471-2105 ; 1471-2105
ISSN (online)	1471-2105
ISSN	1471-2105
DOI	10.1186/s12859-020-03576-5
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Article ; Online: Refined mapping of autoimmune disease associated genetic variants with gene expression suggests an important role for non-coding RNAs.

Journal of autoimmunity

2016 Volume 68, Page(s) 62–74

Abstract: Genome-wide association and fine-mapping studies in 14 autoimmune diseases (AID) have implicated more than 250 loci in one or more of these diseases. As more than 90% of AID-associated SNPs are intergenic or intronic, pinpointing the causal genes is ... ...

Abstract	Genome-wide association and fine-mapping studies in 14 autoimmune diseases (AID) have implicated more than 250 loci in one or more of these diseases. As more than 90% of AID-associated SNPs are intergenic or intronic, pinpointing the causal genes is challenging. We performed a systematic analysis to link 460 SNPs that are associated with 14 AID to causal genes using transcriptomic data from 629 blood samples. We were able to link 71 (39%) of the AID-SNPs to two or more nearby genes, providing evidence that for part of the AID loci multiple causal genes exist. While 54 of the AID loci are shared by one or more AID, 17% of them do not share candidate causal genes. In addition to finding novel genes such as ULK3, we also implicate novel disease mechanisms and pathways like autophagy in celiac disease pathogenesis. Furthermore, 42 of the AID SNPs specifically affected the expression of 53 non-coding RNA genes. To further understand how the non-coding genome contributes to AID, the SNPs were linked to functional regulatory elements, which suggest a model where AID genes are regulated by network of chromatin looping/non-coding RNAs interactions. The looping model also explains how a causal candidate gene is not necessarily the gene closest to the AID SNP, which was the case in nearly 50% of cases.
MeSH term(s)	Autoimmune Diseases/genetics ; Autoimmune Diseases/metabolism ; Autophagy/genetics ; Celiac Disease/genetics ; Celiac Disease/metabolism ; Chromosome Mapping ; Cytokines/metabolism ; Gene Expression ; Gene Expression Regulation ; Genetic Predisposition to Disease ; Genetic Variation ; Genome, Human ; Genome-Wide Association Study ; Genomics ; High-Throughput Nucleotide Sequencing ; Humans ; Linkage Disequilibrium ; Polymorphism, Single Nucleotide ; Quantitative Trait Loci ; RNA, Long Noncoding/genetics ; RNA, Untranslated
Chemical Substances	Cytokines ; RNA, Long Noncoding ; RNA, Untranslated
Language	English
Publishing date	2016-02-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639452-8
ISSN	1095-9157 ; 0896-8411
ISSN (online)	1095-9157
ISSN	0896-8411
DOI	10.1016/j.jaut.2016.01.002
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Article ; Online: Deconvolution of bulk blood eQTL effects into immune cell subpopulations.

Joosten, Irma / Sanna, Serena / Kumar, Vinod / Koenen, Hans J P M / Joosten, Leo A B / Netea, Mihai G / Wijmenga, Cisca / Franke, Lude / Li, Yang

21 ; 1 ; 243 ; BMC bioinformatics ; England

2020

Abstract: A novel planctomycetal strain, designated Pla85_3_4T, was isolated from the surface of wood incubated at the discharge of a wastewater treatment plant in the Warnow river near Rostock, Germany. Cells of the novel strain have a cell envelope architecture ... ...

Abstract	A novel planctomycetal strain, designated Pla85_3_4T, was isolated from the surface of wood incubated at the discharge of a wastewater treatment plant in the Warnow river near Rostock, Germany. Cells of the novel strain have a cell envelope architecture resembling that of Gram-negative bacteria, are round to pear-shaped (length: 2.2 ± 0.4 µm, width: 1.2 ± 0.3 µm), form aggregates and divide by polar budding. Colonies have a cream colour. Strain Pla85_3_4T grows at ranges of 10-30 °C (optimum 26 °C) and at pH 6.5-10.0 (optimum 7.5), and has a doubling time of 26 h. Phylogenetically, strain Pla85_3_4T (DSM 103796T = LMG 29741T) is concluded to represent a novel species of a novel genus within the family Pirellulaceae, for which we propose the name Lignipirellula cremea gen. nov., sp. nov.
Keywords	Cell types ; Deconvolution ; Immune cells ; eQTL
Language	English
Publishing date	2020-06-12
Publisher	BMC
Publishing country	de
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Dissecting the dynamic transcriptional landscape of early T helper cell differentiation into Th1, Th2, and Th1/2 hybrid cells.

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Article: Genetic variation in the non-coding genome: Involvement of micro-RNAs and long non-coding RNAs in disease.

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Article ; Online: Potential impact of celiac disease genetic risk factors on T cell receptor signaling in gluten-specific CD4+ T cells.

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Article: Systematic Prioritization of Candidate Genes in Disease Loci Identifies

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Article ; Online: Systematic Prioritization of Candidate Genes in Disease Loci Identifies as a Master Regulator of IFNγ Signaling in Celiac Disease.

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Article ; Online: Deconvolution of bulk blood eQTL effects into immune cell subpopulations.

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Article ; Online: Refined mapping of autoimmune disease associated genetic variants with gene expression suggests an important role for non-coding RNAs.

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Article ; Online: Deconvolution of bulk blood eQTL effects into immune cell subpopulations.

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