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Article ; Online: The Study of Protein-DNA Interactions in CD4

Hertweck, Arnulf / Jenner, Richard G

Methods in molecular biology (Clifton, N.J.)

2021 Volume 2285, Page(s) 201–216

Abstract: Chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) is an invaluable method to profile of enrichment of histone modifications and transcription factor binding sites across the genome. However, standard ChIP-seq ... ...

Abstract	Chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) is an invaluable method to profile of enrichment of histone modifications and transcription factor binding sites across the genome. However, standard ChIP-seq protocols require large numbers of cells (>10
MeSH term(s)	Animals ; Binding Sites ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; Cells, Cultured ; Chromatin Immunoprecipitation ; DNA/metabolism ; High-Throughput Nucleotide Sequencing ; Humans ; Protein Binding ; Research Design ; Transcription Factors/metabolism ; Workflow
Chemical Substances	Transcription Factors ; DNA (9007-49-2)
Language	English
Publishing date	2021-04-29
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1311-5_17
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Article ; Online: The TH1 cell lineage-determining transcription factor T-bet suppresses TH2 gene expression by redistributing GATA3 away from TH2 genes.

Hertweck, Arnulf / Vila de Mucha, Maria / Barber, Paul R / Dagil, Robert / Porter, Hayley / Ramos, Andres / Lord, Graham M / Jenner, Richard G

Nucleic acids research

2022 Volume 50, Issue 8, Page(s) 4557–4573

Abstract: Lineage-determining transcription factors (LD-TFs) drive the differentiation of progenitor cells into a specific lineage. In CD4+ T cells, T-bet dictates differentiation of the TH1 lineage, whereas GATA3 drives differentiation of the alternative TH2 ... ...

Abstract	Lineage-determining transcription factors (LD-TFs) drive the differentiation of progenitor cells into a specific lineage. In CD4+ T cells, T-bet dictates differentiation of the TH1 lineage, whereas GATA3 drives differentiation of the alternative TH2 lineage. However, LD-TFs, including T-bet and GATA3, are frequently co-expressed but how this affects LD-TF function is not known. By expressing T-bet and GATA3 separately or together in mouse T cells, we show that T-bet sequesters GATA3 at its target sites, thereby removing GATA3 from TH2 genes. This redistribution of GATA3 is independent of GATA3 DNA binding activity and is instead mediated by the T-bet DNA binding domain, which interacts with the GATA3 DNA binding domain and changes GATA3's sequence binding preference. This mechanism allows T-bet to drive the TH1 gene expression program in the presence of GATA3. We propose that redistribution of one LD-TF by another may be a common mechanism that could explain how specific cell fate choices can be made even in the presence of other transcription factors driving alternative differentiation pathways.
MeSH term(s)	Animals ; Cell Lineage ; DNA/metabolism ; GATA3 Transcription Factor/genetics ; GATA3 Transcription Factor/metabolism ; Gene Expression ; Mice ; T-Box Domain Proteins/genetics ; T-Box Domain Proteins/metabolism ; Th2 Cells/cytology ; Th2 Cells/metabolism
Chemical Substances	GATA3 Transcription Factor ; Gata3 protein, mouse ; T-Box Domain Proteins ; T-box transcription factor TBX21 ; DNA (9007-49-2)
Language	English
Publishing date	2022-04-19
Publishing country	England
Document type	Journal Article
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkac258
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Zs.A 1067: Show issues

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Article ; Online: The Th1 cell regulatory circuitry is largely conserved between human and mouse.

Henderson, Stephen / Pullabhatla, Venu / Hertweck, Arnulf / de Rinaldis, Emanuele / Herrero, Javier / Lord, Graham M / Jenner, Richard G

Life science alliance

2021 Volume 4, Issue 11

Abstract: Gene expression programs controlled by lineage-determining transcription factors are often conserved between species. However, infectious diseases have exerted profound evolutionary pressure, and therefore the genes regulated by immune-specific ... ...

Abstract	Gene expression programs controlled by lineage-determining transcription factors are often conserved between species. However, infectious diseases have exerted profound evolutionary pressure, and therefore the genes regulated by immune-specific transcription factors might be expected to exhibit greater divergence. T-bet (Tbx21) is the immune-specific, lineage-specifying transcription factor for T helper type I (Th1) immunity, which is fundamental for the immune response to intracellular pathogens but also underlies inflammatory diseases. We compared T-bet genomic targets between mouse and human CD4
MeSH term(s)	Animals ; Binding Sites/genetics ; Databases, Genetic ; Gene Expression/genetics ; Gene Expression Regulation/genetics ; Genome/genetics ; Humans ; Mice ; Protein Binding/genetics ; T-Box Domain Proteins/genetics ; T-Box Domain Proteins/metabolism ; Th1 Cells/immunology ; Th1 Cells/physiology ; Transcription Factors/genetics ; Transcription Factors/physiology ; Transcriptome/genetics
Chemical Substances	T-Box Domain Proteins ; T-box transcription factor TBX21 ; Transcription Factors
Language	English
Publishing date	2021-09-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2575-1077
ISSN (online)	2575-1077
DOI	10.26508/lsa.202101075
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Article ; Online: Cyclin-dependent Kinase 9 as a Potential Target for Anti-TNF-resistant Inflammatory Bowel Disease.

Omer, Omer S / Hertweck, Arnulf / Roberts, Luke B / Lo, Jonathan W / Clough, Jennie N / Jackson, Ian / Pantazi, Eirini D / Irving, Peter M / MacDonald, Tom T / Pavlidis, Polychronis / Jenner, Richard G / Lord, Graham M

Cellular and molecular gastroenterology and hepatology

2022 Volume 14, Issue 3, Page(s) 625–641

Abstract: Background & aims: Resistance to single cytokine blockade, namely anti-tumor necrosis factor (TNF) therapy, is a growing concern for patients with inflammatory bowel disease (IBD). The transcription factor T-bet is a critical regulator of intestinal ... ...

Abstract	Background & aims: Resistance to single cytokine blockade, namely anti-tumor necrosis factor (TNF) therapy, is a growing concern for patients with inflammatory bowel disease (IBD). The transcription factor T-bet is a critical regulator of intestinal homeostasis, is genetically linked to mucosal inflammation and controls the expression of multiples genes such as the pro-inflammatory cytokines interferon (IFN)-γ and TNF. Inhibiting T-bet may therefore offer a more attractive prospect for treating IBD but remains challenging to target therapeutically. In this study, we evaluate the effect of targeting the transactivation function of T-bet using inhibitors of P-TEFb (CDK9-cyclin T), a transcriptional elongation factor downstream of T-bet. Methods: Using an adaptive immune-mediated colitis model, human colonic lymphocytes from patients with IBD and multiple large clinical datasets, we investigate the effect of cyclin-dependent kinase 9 (CDK9) inhibitors on cytokine production and gene expression in colonic CD4 Results: Systemic CDK9 inhibition led to histological improvement of immune-mediated colitis and was associated with targeted suppression of colonic CD4 Conclusion: Collectively, our findings reveal CDK9 as a potential target for anti-TNF-resistant IBD, which has the potential for rapid translation to the clinic.
MeSH term(s)	Colitis/drug therapy ; Cyclin-Dependent Kinase 9 ; Cytokines/metabolism ; Humans ; Inflammatory Bowel Diseases/drug therapy ; Inflammatory Bowel Diseases/pathology ; Tumor Necrosis Factor Inhibitors
Chemical Substances	Cytokines ; Tumor Necrosis Factor Inhibitors ; CDK9 protein, human (EC 2.7.11.22) ; Cyclin-Dependent Kinase 9 (EC 2.7.11.22)
Language	English
Publishing date	2022-06-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2819778-1
ISSN	2352-345X ; 2352-345X
ISSN (online)	2352-345X
ISSN	2352-345X
DOI	10.1016/j.jcmgh.2022.05.011
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Article ; Online: A population of naive-like CD4

Lo, Jonathan W / de Mucha, Maria Vila / Henderson, Stephen / Roberts, Luke B / Constable, Laura E / Garrido-Mesa, Natividad / Hertweck, Arnulf / Stolarczyk, Emilie / Houlder, Emma L / Jackson, Ian / MacDonald, Andrew S / Powell, Nick / Neves, Joana F / Howard, Jane K / Jenner, Richard G / Lord, Graham M

European journal of immunology

2022 Volume 52, Issue 4, Page(s) 566–581

Abstract: T-bet is the lineage-specifying transcription factor for ... ...

Abstract	T-bet is the lineage-specifying transcription factor for CD4
MeSH term(s)	Animals ; Cell Differentiation ; Gene Expression Regulation ; Lymphocyte Activation ; Mice ; T-Box Domain Proteins/genetics ; T-Box Domain Proteins/metabolism ; T-Lymphocytes, Regulatory/metabolism ; Th1 Cells ; Th17 Cells/metabolism ; Th2 Cells
Chemical Substances	T-Box Domain Proteins
Language	English
Publishing date	2022-02-12
Publishing country	Germany
Document type	Journal Article
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.202149228
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Zs.A 489: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Dominant regulation of long-term allograft survival is mediated by microRNA-142.

Anandagoda, Nelomi / Roberts, Luke B / Willis, Joanna C D / Sarathchandra, Padmini / Xiao, Fang / Jackson, Ian / Hertweck, Arnulf / Kapoor, Puja / Jenner, Richard G / Howard, Jane K / Lord, Graham M

American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons

2020 Volume 20, Issue 10, Page(s) 2715–2727

Abstract: Organ transplantation is often lifesaving, but the long-term deleterious effects of combinatorial immunosuppression regimens and allograft failure cause significant morbidity and mortality. Long-term graft survival in the absence of continuing ... ...

Abstract	Organ transplantation is often lifesaving, but the long-term deleterious effects of combinatorial immunosuppression regimens and allograft failure cause significant morbidity and mortality. Long-term graft survival in the absence of continuing immunosuppression, defined as operational tolerance, has never been described in the context of multiple major histocompatibility complex (MHC) mismatches. Here, we show that miR-142 deficiency leads to indefinite allograft survival in a fully MHC mismatched murine cardiac transplant model in the absence of exogenous immunosuppression. We demonstrate that the cause of indefinite allograft survival in the absence of miR-142 maps specifically to the T cell compartment. Of therapeutic relevance, temporal deletion of miR-142 in adult mice prior to transplantation of a fully MHC mismatched skin allograft resulted in prolonged allograft survival. Mechanistically, miR-142 directly targets Tgfbr1 for repression in regulatory T cells (T
MeSH term(s)	Allografts ; Animals ; Graft Rejection/etiology ; Graft Survival ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; MicroRNAs/genetics ; T-Lymphocytes, Regulatory ; Transplantation Tolerance ; Transplantation, Homologous
Chemical Substances	MicroRNAs ; Mirn142 microRNA, mouse
Language	English
Publishing date	2020-04-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2060594-8
ISSN	1600-6143 ; 1600-6135
ISSN (online)	1600-6143
ISSN	1600-6135
DOI	10.1111/ajt.15907
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Zs.A 5542: Show issues

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Article ; Online: A Crohn's Disease-associated IL2RA Enhancer Variant Determines the Balance of T Cell Immunity by Regulating Responsiveness to IL-2 Signalling.

Goldberg, Rimma / Clough, Jennie N / Roberts, Luke B / Sanchez, Jenifer / Kordasti, Shahram / Petrov, Nedyalko / Hertweck, Arnulf / Lorenc, Anna / Jackson, Ian / Tasker, Scott / Appios, Anna / Omer, Omer / Parkes, Miles / Prescott, Natalie / Jenner, Richard G / Irving, Peter M / Lord, Graham M

Journal of Crohn's & colitis

2021 Volume 15, Issue 12, Page(s) 2054–2065

Abstract: Background and aims: Differential responsiveness to interleukin [IL]-2 between effector CD4+ T cells [Teff] and regulatory T cells [Treg] is a fundamental mechanism of immunoregulation. The single nucleotide polymorphism [SNP] rs61839660, located within ...

Abstract	Background and aims: Differential responsiveness to interleukin [IL]-2 between effector CD4+ T cells [Teff] and regulatory T cells [Treg] is a fundamental mechanism of immunoregulation. The single nucleotide polymorphism [SNP] rs61839660, located within IL2RA [CD25], has been associated with the development of Crohn's disease [CD]. We sought to identify the T cell immune phenotype of IBD patients who carry this SNP. Methods: Teff and Treg were isolated from individuals homozygous [TT], heterozygous [CT], or wild-type [CC] for the minor allele at rs61839660, and used for phenotyping [flow cytometry, Cytometry Time Of Flight] functional assays or T cell receptor [TCR] sequencing. Phosphorylation of signal transducer and activator of transcription 5 [STAT5] was assessed in response to IL-2, IL-7, and in the presence of basiliximab, a monoclonal antibody directed against CD25. Teff pro-inflammatory cytokine expression levels were assessed by reverse transcription quantitative polymerase chain reaction after IL-2 and/or TCR stimulation. Results: Presence of the minor T allele enhances CD25 expression, leading to increased STAT5 phosphorylation and pro-inflammatory cytokine transcript expression by Teff in response to IL-2 stimulation in vitro. Teff from TT individuals demonstrate a more activated gut homing phenotype. TCR sequencing analysis suggests that TT patients may have a reduced clonal capacity to mount an optimal regulatory T cell response. Conclusions: rs61839660 regulates the responsiveness of T cells to IL-2 signalling by modulating CD25 expression. As low-dose IL-2 is being trialled as a selective Treg modulator in CD, these findings highlight the potential for adverse effects in patients with this genotype.
MeSH term(s)	CD4-Positive T-Lymphocytes/immunology ; Case-Control Studies ; Crohn Disease/genetics ; Crohn Disease/immunology ; Databases, Factual ; Female ; Humans ; Immunophenotyping ; Interleukin-2/immunology ; Interleukin-2 Receptor alpha Subunit/immunology ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Signal Transduction ; State Medicine ; T-Lymphocytes, Regulatory/immunology ; United Kingdom
Chemical Substances	IL2 protein, human ; IL2RA protein, human ; Interleukin-2 ; Interleukin-2 Receptor alpha Subunit
Language	English
Publishing date	2021-06-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2390120-2
ISSN	1876-4479 ; 1873-9946
ISSN (online)	1876-4479
ISSN	1873-9946
DOI	10.1093/ecco-jcc/jjab103
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Zs.A 6634: Show issues

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Article ; Online: microRNA-142-mediated repression of phosphodiesterase 3B critically regulates peripheral immune tolerance.

Anandagoda, Nelomi / Willis, Joanna Cd / Hertweck, Arnulf / Roberts, Luke B / Jackson, Ian / Gökmen, M Refik / Jenner, Richard G / Howard, Jane K / Lord, Graham M

The Journal of clinical investigation

2019 Volume 129, Issue 3, Page(s) 1257–1271

Abstract: Tregs play a fundamental role in immune tolerance via control of self-reactive effector T cells (Teffs). This function is dependent on maintenance of a high intracellular cAMP concentration. A number of microRNAs are implicated in the maintenance of ... ...

Abstract	Tregs play a fundamental role in immune tolerance via control of self-reactive effector T cells (Teffs). This function is dependent on maintenance of a high intracellular cAMP concentration. A number of microRNAs are implicated in the maintenance of Tregs. In this study, we demonstrate that peripheral immune tolerance is critically dependent on posttranscriptional repression of the cAMP-hydrolyzing enzyme phosphodiesterase-3b (Pde3b) by microRNA-142-5p (miR-142-5p). In this manner, miR-142-5p acts as an immunometabolic regulator of intracellular cAMP, controlling Treg suppressive function. Mir142 was associated with a super enhancer bound by the Treg lineage-determining transcription factor forkhead box P3 (FOXP3), and Treg-specific deletion of miR-142 in mice (TregΔ142) resulted in spontaneous, lethal, multisystem autoimmunity, despite preserved numbers of phenotypically normal Tregs. Pharmacological inhibition and genetic ablation of PDE3B prevented autoimmune disease and reversed the impaired suppressive function of Tregs in TregΔ142 animals. These findings reveal a critical molecular switch, specifying Treg function through the modulation of a highly conserved, cell-intrinsic metabolic pathway. Modulation of this pathway has direct relevance to the pathogenesis and treatment of autoimmunity and cancer.
MeSH term(s)	Animals ; Autoimmune Diseases/genetics ; Autoimmune Diseases/immunology ; Autoimmune Diseases/pathology ; Cyclic AMP/genetics ; Cyclic AMP/immunology ; Cyclic Nucleotide Phosphodiesterases, Type 3/genetics ; Cyclic Nucleotide Phosphodiesterases, Type 3/immunology ; Gene Expression Regulation, Enzymologic/genetics ; Gene Expression Regulation, Enzymologic/immunology ; Immune Tolerance ; Mice ; Mice, Transgenic ; MicroRNAs/genetics ; MicroRNAs/immunology ; Second Messenger Systems/genetics ; Second Messenger Systems/immunology ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/pathology
Chemical Substances	MicroRNAs ; Mirn142 microRNA, mouse ; Cyclic AMP (E0399OZS9N) ; Cyclic Nucleotide Phosphodiesterases, Type 3 (EC 3.1.4.17) ; Pde3b protein, mouse (EC 3.1.4.17)
Language	English
Publishing date	2019-02-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI124725
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Article ; Online: Genetic variants alter T-bet binding and gene expression in mucosal inflammatory disease.

Soderquest, Katrina / Hertweck, Arnulf / Giambartolomei, Claudia / Henderson, Stephen / Mohamed, Rami / Goldberg, Rimma / Perucha, Esperanza / Franke, Lude / Herrero, Javier / Plagnol, Vincent / Jenner, Richard G / Lord, Graham M

PLoS genetics

2017 Volume 13, Issue 2, Page(s) e1006587

Abstract: The polarization of CD4+ T cells into distinct T helper cell lineages is essential for protective immunity against infection, but aberrant T cell polarization can cause autoimmunity. The transcription factor T-bet (TBX21) specifies the Th1 lineage and ... ...

Abstract	The polarization of CD4+ T cells into distinct T helper cell lineages is essential for protective immunity against infection, but aberrant T cell polarization can cause autoimmunity. The transcription factor T-bet (TBX21) specifies the Th1 lineage and represses alternative T cell fates. Genome-wide association studies have identified single nucleotide polymorphisms (SNPs) that may be causative for autoimmune diseases. The majority of these polymorphisms are located within non-coding distal regulatory elements. It is considered that these genetic variants contribute to disease by altering the binding of regulatory proteins and thus gene expression, but whether these variants alter the binding of lineage-specifying transcription factors has not been determined. Here, we show that SNPs associated with the mucosal inflammatory diseases Crohn's disease, ulcerative colitis (UC) and celiac disease, but not rheumatoid arthritis or psoriasis, are enriched at T-bet binding sites. Furthermore, we identify disease-associated variants that alter T-bet binding in vitro and in vivo. ChIP-seq for T-bet in individuals heterozygous for the celiac disease-associated SNPs rs1465321 and rs2058622 and the IBD-associated SNPs rs1551398 and rs1551399, reveals decreased binding to the minor disease-associated alleles. Furthermore, we show that rs1465321 is an expression quantitative trait locus (eQTL) for the neighboring gene IL18RAP, with decreased T-bet binding associated with decreased expression of this gene. These results suggest that genetic polymorphisms may predispose individuals to mucosal autoimmune disease through alterations in T-bet binding. Other disease-associated variants may similarly act by modulating the binding of lineage-specifying transcription factors in a tissue-selective and disease-specific manner.
MeSH term(s)	Animals ; Binding Sites/genetics ; Blotting, Western ; CD4-Positive T-Lymphocytes/metabolism ; Celiac Disease/genetics ; Celiac Disease/metabolism ; Cells, Cultured ; Colitis, Ulcerative/genetics ; Colitis, Ulcerative/metabolism ; Crohn Disease/genetics ; Crohn Disease/metabolism ; Gene Expression ; Genetic Predisposition to Disease/genetics ; Genome-Wide Association Study/methods ; Humans ; Interleukin-18 Receptor beta Subunit/genetics ; Interleukin-18 Receptor beta Subunit/metabolism ; Mice, Knockout ; Polymorphism, Single Nucleotide ; Protein Binding/genetics ; Regulatory Sequences, Nucleic Acid/genetics ; T-Box Domain Proteins/genetics ; T-Box Domain Proteins/metabolism ; Th1 Cells/metabolism
Chemical Substances	IL18RAP protein, human ; Interleukin-18 Receptor beta Subunit ; T-Box Domain Proteins ; T-box transcription factor TBX21
Language	English
Publishing date	2017-02-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1006587
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Article ; Online: T-bet Activates Th1 Genes through Mediator and the Super Elongation Complex.

Hertweck, Arnulf / Evans, Catherine M / Eskandarpour, Malihe / Lau, Jonathan C H / Oleinika, Kristine / Jackson, Ian / Kelly, Audrey / Ambrose, John / Adamson, Peter / Cousins, David J / Lavender, Paul / Calder, Virginia L / Lord, Graham M / Jenner, Richard G

Cell reports

2016 Volume 15, Issue 12, Page(s) 2756–2770

Abstract: The transcription factor T-bet directs Th1 cell differentiation, but the molecular mechanisms that underlie this lineage-specific gene regulation are not completely understood. Here, we show that T-bet acts through enhancers to allow the recruitment of ... ...

Abstract	The transcription factor T-bet directs Th1 cell differentiation, but the molecular mechanisms that underlie this lineage-specific gene regulation are not completely understood. Here, we show that T-bet acts through enhancers to allow the recruitment of Mediator and P-TEFb in the form of the super elongation complex (SEC). Th1 genes are occupied by H3K4me3 and RNA polymerase II in Th2 cells, while T-bet-mediated recruitment of P-TEFb in Th1 cells activates transcriptional elongation. P-TEFb is recruited to both genes and enhancers, where it activates enhancer RNA transcription. P-TEFb inhibition and Mediator and SEC knockdown selectively block activation of T-bet target genes, and P-TEFb inhibition abrogates Th1-associated experimental autoimmune uveitis. T-bet activity is independent of changes in NF-κB RelA and Brd4 binding, with T-bet- and NF-κB-mediated pathways instead converging to allow P-TEFb recruitment. These data provide insight into the mechanism through which lineage-specifying factors promote differentiation of alternative T cell fates.
MeSH term(s)	Animals ; Cell Lineage/genetics ; Enhancer Elements, Genetic/genetics ; Gene Expression Regulation ; Humans ; Mice, Inbred C57BL ; Nuclear Proteins/metabolism ; Positive Transcriptional Elongation Factor B/metabolism ; Protein Binding/genetics ; RNA/genetics ; RNA/metabolism ; T-Box Domain Proteins/metabolism ; Th1 Cells/metabolism ; Th2 Cells/metabolism ; Transcription Elongation, Genetic ; Transcription Factor RelA/metabolism ; Transcription Factors/metabolism ; Uveitis/genetics
Chemical Substances	Brd4 protein, mouse ; Nuclear Proteins ; T-Box Domain Proteins ; T-box transcription factor TBX21 ; Transcription Factor RelA ; Transcription Factors ; RNA (63231-63-0) ; Positive Transcriptional Elongation Factor B (EC 2.7.11.-)
Language	English
Publishing date	2016-06-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2016.05.054
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