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  • 1
    Language: English
    In: FASEB journal : official publication of the Federation of American Societies for Experimental Biology, September 2014, Vol.28(9), pp.4068-76
    Description: Folate intake during pregnancy may affect the regulation of DNA methylation during fetal development. The genomic regions in the offspring that may be sensitive to folate exposure during in utero development have not been characterized. Using genome-scale profiling, we investigated DNA methylation in 2 immune cell types (CD4(+) and antigen-presenting cells) isolated from neonatal cord blood, selected on the basis of in utero folate exposure. High-folate (HF; n=11) and low-folate (LF; n=12) groups were selected from opposite extremes of maternal serum folate levels measured in the last trimester of pregnancy. A comparison of these groups revealed differential methylation at 7 regions across the genome. By far, the biggest effect observed was hypomethylation of a 923 bp region 3 kb upstream of the ZFP57 transcript, a regulator of DNA methylation during development, observed in both cell types. Levels of H3/H4 acetylation at ZFP57 promoter and ZFP57 mRNA expression were higher in CD4(+) cells in the HF group relative to the LF group. Hypomethylation at this region was replicated in an independent sample set. These data suggest that exposure to folate has effects on the regulation of DNA methylation during fetal development, and this may be important for health and disease.
    Keywords: T Cells ; Antigen-Presenting Cells ; Developmental Programming ; Epigenetics ; Neonate ; DNA Methylation ; Gene Expression Profiling ; Genome, Human ; Genomic Imprinting ; DNA-Binding Proteins -- Genetics ; Fetal Development -- Genetics ; Folic Acid -- Metabolism ; Transcription Factors -- Genetics
    ISSN: 08926638
    E-ISSN: 1530-6860
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  • 2
    Language: English
    In: The Journal of Allergy and Clinical Immunology, July 2015, Vol.136(1), pp.200-202
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jaci.2015.01.027 Byline: Hani Harb, Diana Raedler, Nikolaus Ballenberger, Andreas Bock, Dorthe A. Kesper, Harald Renz, Bianca Schaub Author Affiliation: (a) Institute of Laboratory Medicine, Pathobiochemistry and Molecular Diagnostics, Philipps University, Marburg, Germany (b) Department of Pulmonary and Allergy, University Children's Hospital Munich, LMU, Munich, Germany (c) German Center for Lung Research (DZL), Munich, Germany Article Note: (footnote) This study was funded by the Sonderforschungsbereich-Transregio 22 (SFB-TR22), Deutsche Forschungsgemeinschaft (DFG), Else-Kroner-Fresenius-Stiftung (EKFS), Universities of Giessen and Marburg Lung Center (UGMLC), and Deutsches Zentrum fur Lungenforschung (DZL)., Disclosure of potential conflict of interest: B. Schaub has received research support from the German Research Foundation (DFG SFB-TR22). The rest of the authors declare that they have no relevant conflicts of interest.
    Keywords: Medicine
    ISSN: 0091-6749
    E-ISSN: 1097-6825
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  • 3
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 10 September 2013, Vol.110(37), pp.15019-24
    Description: Robust cytotoxic CD8(+) T-cell response is important for immunity to intracellular pathogens. Here, we show that the transcription factor IFN Regulatory Factor 4 (IRF4) is crucial for the protective CD8(+) T-cell response to the intracellular bacterium Listeria monocytogenes. IRF4-deficient (Irf4(-/-)) mice could not clear L. monocytogenes infection and generated decreased numbers of L. monocytogenes-specific CD8(+) T cells with impaired effector phenotype and function. Transfer of wild-type CD8(+) T cells into Irf4(-/-) mice improved bacterial clearance, suggesting an intrinsic defect of CD8(+) T cells in Irf4(-/-) mice. Following transfer into wild-type recipients, Irf4(-/-) CD8(+) T cells became activated and showed initial proliferation upon L. monocytogenes infection. However, these cells could not sustain proliferation, produced reduced amounts of IFN-γ and TNF-α, and failed to acquire cytotoxic function. Forced IRF4 expression in Irf4(-/-) CD8(+) T cells rescued the defect. During acute infection, Irf4(-/-) CD8(+) T cells demonstrated diminished expression of B lymphocyte-induced maturation protein-1 (Blimp-1), inhibitor of DNA binding (Id)2, and T-box expressed in T cells (T-bet), transcription factors programming effector-cell generation. IRF4 was essential for expression of Blimp-1, suggesting that altered regulation of Blimp-1 contributes to the defects of Irf4(-/-) CD8(+) T cells. Despite increased levels of B-cell lymphoma 6 (BCL-6), Eomesodermin, and Id3, Irf4(-/-) CD8(+) T cells showed impaired memory-cell formation, indicating additional functions for IRF4 in this process. As IRF4 governs B-cell and CD4(+) T-cell differentiation, the identification of its decisive role in peripheral CD8(+) T-cell differentiation, suggests a common regulatory function for IRF4 in adaptive lymphocytes fate decision.
    Keywords: Interferon Regulatory Factors -- Immunology ; T-Lymphocytes, Cytotoxic -- Immunology
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 4
    Language: English
    In: The Journal of Allergy and Clinical Immunology, June 2012, Vol.129(6), pp.1602-1610.e6
    Description: Epigenetic changes in DNA methylation have recently been demonstrated to be involved in effector T-cell polarization, resulting in differential secretion of T 1 and T 2 cytokines. However, the contribution to the development of a chronic inflammatory phenotype remains still unclear. We sought to investigate changes in DNA methylation in marker genes of T-cell subsets during allergen sensitization/challenge and their influence on the development of an allergic airway inflammatory response. The relationship between changes in DNA methylation and phenotype development were examined in a well-established model of experimental asthma. DNA methylation was investigated at genomic loci associated with T 1 ( promoter) or T 2 (conserved noncoding sequence 1 ) cytokine production by using bisulfite pyrosequencing. Analysis of CD4 T cells revealed a significant increase in DNA methylation at the promoter after allergen sensitization/challenge, which correlated with decreased IFN-γ cytokine expression, whereas only minor changes were observed at the locus. Furthermore, the increase in DNA methylation at the promoter could be reversed with a DNA methyltransferase (DNMT) inhibitor and with beneficial effects on sensitization status and allergic phenotype. The specific importance of the DNA methylation status in CD4 T cells could be confirmed by using adoptive transfer experiments. We here report the novel finding that epigenetic regulation in T cells contributes to the development of experimental asthma and can be targeted pharmacologically.
    Keywords: Epigenetics ; T Cells ; Experimental Asthma ; Medicine
    ISSN: 0091-6749
    E-ISSN: 1097-6825
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  • 5
    Language: English
    In: Molecular and Cellular Endocrinology, 31 March 2012, Vol.351(1), pp.19-27
    Description: ► Shh signal produced by partially differentiated outer cortical/zona glomerulosa cells. ► Signal received only by non-cortical mesenchyme cells, predominantly in capsule. ► Capsule and cortex growth need Shh; zonation and steroidogenic differentiation do not. ► Pallister–Hall syndrome mice ( ) have adrenal glands. ► Lineage analyses show and expression mark cortical stem/progenitor cells. It has been speculated for a number of years that Sonic hedgehog (Shh) signaling plays an important role in adrenal development. Over the past two years several reports have described the expression and function of pathway genes in the adrenal cortex, using primarily mouse models. The key findings are that Shh signals produced by a population of partially differentiated cortical cells located in the outer cortex/zona glomerulosa are received by non-cortical mesenchymal cells located predominantly in the overlying capsule. This signal is required for growth of both the capsule and the cortex, but not for cortical zonation or steroidogenic cell differentiation. Using molecular genetic tools to define the adrenocortical cell lineages that are descended from both Shh signaling and receiving cells, both capsule and cortical cells were found to have properties of adrenocortical stem and/or progenitor cells. Here we place these observations within the context of prior studies on adrenal development, postnatal adrenal maintenance and adrenocortical stem/progenitor cell lineages.
    Keywords: Adrenal Cortex ; Steroidogenic ; Sonic Hedgehog ; Gli ; Development ; Signaling ; Pallister–Hall Syndrome ; Medicine ; Anatomy & Physiology
    ISSN: 0303-7207
    E-ISSN: 1872-8057
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  • 6
    Language: German
    In: Allergo Journal, 10/2013, Vol.22(7), pp.464-470
    Description: Wie auch andere chronische Erkrankungen des Menschen sind Allergien nicht monokausal begründet — vielmehr entstehen sie durch das Zusammenwirken vielfältiger exogener und endogener Faktoren mit dem Immunsystem. In Zwillingsstudien konnte belegt werden, dass eine genetische Komponente an diesem Zusammenspiel beteiligt ist. Die schnelle Zunahme von Allergien innerhalb der letzten sechs Dekaden deutete darauf hin, dass Umweltexpositionen ebenfalls ursächlich an der Initiation allergischer Entzündungen beteiligt sind. Die epidemiologische Erforschung der Allergogenese führte zur Identifikation von Risiko- und Schutzfaktoren aus der Umwelt, die neue Ansätze für die Prävention und Therapie bieten könnten. Darüber hinaus hat die Translation epidemiologischer Befunde in tierexperimentelle Modelle den Zugang zu den Mechanismen eröffnet, die der Allergieentstehung zugrunde liegen. Zwei Konzepte bildeten die Grundlage für ein neues Verständnis der frühen Immunprogrammierung: erstens die Hygienehypothese, die die Bedeutung mikrobieller Stimuli in der Entwicklung der tolerogenen Immunantwort unterstreicht, und zweitens die Barker-Hypothese, die die Weichenstellung für chronische Krankheitsprozesse im Alter bereits in der Pränatalphase ansiedelt.As other human chronic diseases allergies are not of mono-causative etiology — these conditions develop by a complex misguided interplay between exogenous and endogenous determinants and the developing immune system. Twin studies substantiated genetic factors as basic determinants involved in this interplay. The rapid increase of allergic disorders within the last six decades pointed out to a causative contribution of environmental exposures as crucial in initiating allergic inflammation. Epidemiological research focusing on the onset of allergies led to the identification of risk and protective environmental factors, which might offer new approaches for prevention and therapy. Moreover, translation of epidemiological evidence into animal models provided access to immune mechanisms underlying the development of allergies. Two concepts built the fundament for a new understanding of early immune programming: (1) The hygiene hypothesis, which emphasizes the impact of microbial stimuli on the development of a tolerogenic immune response and (2) the Barker-hypothesis, which allocates the onset of chronic disease already in utero.
    Keywords: Medicine & Public Health ; General Practice / Family Medicine ; Allergie ; Asthmaentstehung ; Umweltfaktoren ; Mikrobielle Stimuli ; Hygienehypothese ; Allergy ; Asthma Development ; Environmental Factors ; Microbial Stimuli ; Hygiene Hypothesis;
    ISSN: 0941-8849
    E-ISSN: 2195-6405
    Source: Springer (via CrossRef)
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  • 7
    Language: German
    In: Allergo Journal, 2013, Vol.22(7), pp.464-470
    Description: Wie auch andere chronische Erkrankungen des Menschen sind Allergien nicht monokausal begründet — vielmehr entstehen sie durch das Zusammenwirken vielfältiger exogener und endogener Faktoren mit dem Immunsystem. In Zwillingsstudien konnte belegt werden, dass eine genetische Komponente an diesem Zusammenspiel beteiligt ist. Die schnelle Zunahme von Allergien innerhalb der letzten sechs Dekaden deutete darauf hin, dass Umweltexpositionen ebenfalls ursächlich an der Initiation allergischer Entzündungen beteiligt sind. Die epidemiologische Erforschung der Allergogenese führte zur Identifikation von Risiko- und Schutzfaktoren aus der Umwelt, die neue Ansätze für die Prävention und Therapie bieten könnten. Darüber hinaus hat die Translation epidemiologischer Befunde in tierexperimentelle Modelle den Zugang zu den Mechanismen eröffnet, die der Allergieentstehung zugrunde liegen. Zwei Konzepte bildeten die Grundlage für ein neues Verständnis der frühen Immunprogrammierung: erstens die Hygienehypothese, die die Bedeutung mikrobieller Stimuli in der Entwicklung der tolerogenen Immunantwort unterstreicht, und zweitens die Barker-Hypothese, die die Weichenstellung für chronische Krankheitsprozesse im Alter bereits in der Pränatalphase ansiedelt. As other human chronic diseases allergies are not of mono-causative etiology — these conditions develop by a complex misguided interplay between exogenous and endogenous determinants and the developing immune system. Twin studies substantiated genetic factors as basic determinants involved in this interplay. The rapid increase of allergic disorders within the last six decades pointed out to a causative contribution of environmental exposures as crucial in initiating allergic inflammation. Epidemiological research focusing on the onset of allergies led to the identification of risk and protective environmental factors, which might offer new approaches for prevention and therapy. Moreover, translation of epidemiological evidence into animal models provided access to immune mechanisms underlying the development of allergies. Two concepts built the fundament for a new understanding of early immune programming: (1) The hygiene hypothesis, which emphasizes the impact of microbial stimuli on the development of a tolerogenic immune response and (2) the Barker-hypothesis, which allocates the onset of chronic disease already in utero.
    Keywords: Allergy ; asthma development ; environmental factors ; microbial stimuli ; hygiene hypothesis
    ISSN: 0941-8849
    E-ISSN: 2195-6405
    Source: Springer Science & Business Media B.V.
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  • 8
    Language: English
    In: Developmental dynamics : an official publication of the American Association of Anatomists, June 2010, Vol.239(6), pp.1818-26
    Description: Signaling of Indian hedgehog (Ihh), one of the key regulators of endochondral ossification is mediated by transcription factors of the Gli family, Gli1, Gli2, and Gli3. Gli3 and to a lesser extent Gli2 can be proteolytically processed into short repressor proteins. Upon Ihh signaling, processing is inhibited and the full-length proteins function as activators of transcription. Gli3 has been shown to mainly act as a repressor of Ihh target genes in chondrocytes, but the role of other Gli isoforms is less clear. Analyzing mouse mutants deficient for Ihh;Gli2 or Gli3;Gli2, we show here that the Gli2 repressor has no detectable function in chondrocyte or osteoblast differentiation. Instead, Gli2 seems to act as an activator to fully induce the expression of Ihh target genes in skeletal tissues. Furthermore, we show that, in the absence of Gli3, the activator function of Gli2 is sufficient to induce Ihh-dependent osteoblast differentiation.
    Keywords: Cell Differentiation -- Physiology ; Osteogenesis -- Physiology ; Proteins -- Metabolism
    ISSN: 10588388
    E-ISSN: 1097-0177
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  • 9
    Language: English
    In: Developmental Dynamics, June 2010, Vol.239(6), pp.1818-1826
    Description: Signaling of Indian hedgehog (Ihh), one of the key regulators of endochondral ossification is mediated by transcription factors of the Gli family, Gli1, Gli2, and Gli3. Gli3 and to a lesser extent Gli2 can be proteolytically processed into short repressor proteins. Upon Ihh signaling, processing is inhibited and the full‐length proteins function as activators of transcription. Gli3 has been shown to mainly act as a repressor of Ihh target genes in chondrocytes, but the role of other Gli isoforms is less clear. Analyzing mouse mutants deficient for or , we show here that the Gli2 repressor has no detectable function in chondrocyte or osteoblast differentiation. Instead, Gli2 seems to act as an activator to fully induce the expression of Ihh target genes in skeletal tissues. Furthermore, we show that, in the absence of Gli3, the activator function of Gli2 is sufficient to induce Ihh‐dependent osteoblast differentiation. Developmental Dynamics 239:1818–1826, 2010. © 2010 Wiley‐Liss, Inc.
    Keywords: Gli2 ; Gli3 ; Indian Hedgehog Ihh ; Cartilage ; Ossification ; Bone ; Osteoblast
    ISSN: 1058-8388
    E-ISSN: 1097-0177
    Source: John Wiley & Sons, Inc.
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  • 10
    Language: English
    In: Frontiers in Physiology, 01 May 2012, Vol.3
    Description: Greig cephalopolysyndactyly syndrome (GCPS) is an autosomal dominant disorder with polydactyly and syndactyly of the limbs and a broad spectrum of craniofacial abnormalities. Craniosynostosis of the metopic suture (interfrontal suture in mice) is an important, rare feature associated with GCPS. GCPS is caused by mutations in the transcription factor GLI3, which regulates Hedgehog signaling. The Gli3 null allele (Gli3Xt-J/Xt-J) mouse largely phenocopies the human syndrome with the mice exhibiting polydactyly and several craniofacial abnormalities. Here we show that Gli3Xt-J/Xt-J mice exhibit ectopic ossification in the interfrontal suture and in the most severe cases the suture fuses already prior to birth. We show that abnormalities in frontal bones occur early in calvarial development, before the establishment of the interfrontal suture. Thus in this aspect the Gli3Xt-J/Xt-J mouse mimics GCPS patients with GLI3 mutations and metopic suture abnormalities. It provides a model for the metopic suture pathology that can occur in GCPS.
    Keywords: Developmental Biology ; Craniosynostosis ; Gli3 ; Bone ; Suture
    E-ISSN: 1664-042X
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