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Sen2021 - HTimmR - A generic human CD4+ T-cell model

ABSTRACT: A generic genome-scale metabolic model (GEMs) of human CD4+ T-cells. Several cell-specific GEMs for CD4+ T-cell subsets such as Th1, Th2, Th17 and iTreg cells derived from "HTimmR" are included as additional files. The model formats are compatible with RAVEN v.2.0 toolbox.

SUBMITTER: Partho Sen

PROVIDER: MODEL2101270002 | BioModels | 2023-03-29

REPOSITORIES: BioModels

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			Action	DRS
	MODEL2101270002?filename=HTimmR.xml	Xml
	MODEL2101270002?filename=Th1.xml	Xml
	MODEL2101270002?filename=Th17.xml	Xml
	MODEL2101270002?filename=Th2.xml	Xml
	MODEL2101270002?filename=Thp.xml	Xml

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Publications

Quantitative genome-scale metabolic modeling of human CD4<sup>+</sup> T cell differentiation reveals subset-specific regulation of glycosphingolipid pathways.

Sen Partho P Andrabi Syed Bilal Ahmad SBA Buchacher Tanja T Khan Mohd Moin MM Kalim Ubaid Ullah UU Lindeman Tuomas Mikael TM Alves Marina Amaral MA Hinkkanen Victoria V Kemppainen Esko E Dickens Alex M AM Rasool Omid O Hyötyläinen Tuulia T Lahesmaa Riitta R Orešič Matej M

Cell reports 20211101 6

T cell activation, proliferation, and differentiation involve metabolic reprogramming resulting from the interplay of genes, proteins, and metabolites. Here, we aim to understand the metabolic pathways involved in the activation and functional differentiation of human CD4<sup>+</sup> T cell subsets (T helper [Th]1, Th2, Th17, and induced regulatory T [iTreg] cells). Here, we combine genome-scale metabolic modeling, gene expression data, and targeted and non-targeted lipidomics experiments, toget ...[more]

PMID: 34758307

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Project description:Functionally distinct CD4+ helper T (Th) cell subsets, such as Th1, Th2, Th17, and regulatory T cells (Treg), play a pivotal role in the host-defense against pathogen invasion and the pathogenesis of inflammatory disorders. In this project, DIA-MS-based proteome analysis was performed on naïve CD4+ T, Th0, Th1, Th2, Th17 and iTreg cells using Q Exactive HF-X (Thermo Fisher Scientific) to search for proteins that differ among the cell subsets.

2023-01-04 | PXD036065 | JPOST Repository

Profiling of human CD4+ T subsets identifies a Th2-specific non-coding RNA GATA3-AS1

Project description:Host defense against diverse pathogens involves the recruitment and differentiation of CD4+ T effector subsets including T helper 1 (Th1), Th2, Th17 and induced regulatory T (Treg) cells. Surface phenotype studies have revealed subset-specific surface markers for the identification and purification of human primary CD4+ T effector subsets. In the present study, we aimed to characterize the mRNA and large intergenic non-coding RNA (lincRNA) expression differences between human primary CD4+ T effector subsets and identify potential subset-specific genes. To achieve this goal, mRNA and lincRNA microarray profiling of flow cytometry-sorted human primary Th1, Th2, Th17 and Treg cells was performed. Principal component and pathway analyses revealed subset-specific gene expression patterns. A Th2-specific lincRNA, GATA3-AS1, also termed FLJ45983, was identified in primary immune cells and tissues, as well as in in vitro polarized CD4+ T effector subsets. Further analysis showed that GATA3-AS1 was a potential diagnostic marker in allergy, a Th2-associated disease. This first systematic genome-wide analysis of gene expression differences between primary CD4+ T effector subsets may help to identify novel regulatory protein-coding genes and lincRNAs regulating CD4+ T cell subset differentiation, as well as potential diagnostic markers. As an example, we identified a GATA3-associated Th2-specific marker lincRNA GATA3-AS1. Gene expression microarray analysis of flow-cytometry sorted human primary naÃ¯ve CD4+ T cells, CD4+ T central memory cells, Th1, Th2, Th17 and Treg cells from buffy coat of four healthy controls Gene expression microarray analysis was performed using SurePrint G3 Human Gene Expression 8X60K microarray.

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JunB regulates the common and lineage-specific transcriptional programs of distinct CD4+ effector T cells

Project description:IRF4 is critical for differentiation of various CD4+ effector T cells, such as T helper 1 (Th1), Th2, and Th17 subsets, through interaction with BATF-containing AP-1 heterodimers. A major BATF heterodimeric partner, JunB, regulates Th17 differentiation, but the role of JunB in other CD4+ effector T subsets is not fully understood. Here we demonstrate that JunB is essential for accumulation of Th1 and Th2 cells, as well as Th17 cells, both in vitro and in vivo. In mice immunized with lipopolysaccharide (LPS), papain, or complete Freund’s adjuvant (CFA), that induce predominantly Th1, Th2 and Th17 cells, respectively, accumulation of antigen-primed, Junb-deficient CD4+ T cells is significantly impaired. Loss of JunB decreases viability of cells activated under Th1-, Th2-, and Th17-polarizing conditions. RNA-sequencing (RNA-seq) and chromatin immunoprecipitation sequencing (ChIP-seq) reveal that JunB directly regulates expression of various genes that are commonly induced in priming of naïve CD4+ T cells, including a pro-apoptotic gene Bcl2l11 (encoding Bim), and genes that are specifically induced in Th1, Th2, and Th17 cells. Furthermore, JunB colocalizes with BATF and IRF4 at genomic regions for approximately half of JunB direct target genes. Taken together, JunB, in collaboration with BATF and IRF4, serves a critical function in differentiation of diverse CD4+ T cells by controlling common and lineage-specific gene expression.

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Profiling of human CD4+ T subsets identifies a Th2-specific non-coding RNA GATA3-AS1

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Gene expression analysis of CD4+ and CD4- ILC1 subsets by RNAseq

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Effect of Ibrutinib on the gene expression of CD4+ cells from patients with Peripheral T-cell lymphoma (PTCL)

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