0000000000413376

AUTHOR

Petra Adams

showing 3 related works from this author

A genetic basis for IFN-gamma production and T-bet expression in humans.

2005

Abstract Th1 and Th2 cytokines secreted by polarized effector T cells play a pivotal role in the development of autoimmune and allergic diseases. However, the genetic basis of cytokine production by T lymphocytes in humans is poorly understood. In this study, we investigated the genetic contribution to cytokine production and regulation of T cell-specific transcription factors in a prospective twin study. We found a substantial genetic contribution to the production of Th1 cytokines such as IFN-γ and TNF-α with heritabilities of 0.85 (95% confidence intervals, 0.74–0.95) and 0.72 (0.50–0.93), respectively, whereas no genetic influence on production of the Th2 signature cytokine IL-4 was obs…

AdultMaleAdolescentmedicine.medical_treatmentImmunologyGATA3 Transcription FactorBiologyBody Mass IndexInterferon-gammaSex FactorsGenetic variationmedicineImmunology and AllergyHumansProspective StudiesGeneTranscription factorCells CulturedAgedGeneticsNFATC Transcription FactorsEffectorTumor Necrosis Factor-alphaAge FactorsNF-kappa BNFATHeritabilityMiddle AgedTwin studyCytokineImmunologyFemaleInterleukin-4T-Box Domain ProteinsTranscription FactorsJournal of immunology (Baltimore, Md. : 1950)
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Balanced Bcl-3 expression in murine CD4+T cells is required for generation of encephalitogenic Th17 cells

2017

The function of NF-κB family members is controlled by multiple mechanisms including the transcriptional regulator Bcl-3, an atypical member of the IκB family. By using a murine model of conditional Bcl-3 overexpression specifically in T cells, we observed impairment in the development of Th2, Th1 and Th17 cells. High expression of Bcl-3 promoted CD4+ T-cell survival, but at the same time suppressed proliferation in response to TCR stimulation, resulting in reduced CD4+ T-cell expansion. As a consequence, T cell specific overexpression of Bcl-3 led to reduced inflammation in the small intestine of mice applied with anti-CD3 in a model of gut inflammation. Moreover, impaired Th17-cell develop…

0301 basic medicineT cellMultiple sclerosisImmunologyT-cell receptorStimulationInflammationNF-κBBiologymedicine.diseaseSmall intestineCell biology03 medical and health scienceschemistry.chemical_compound030104 developmental biologymedicine.anatomical_structurechemistryImmunologymedicineTranscriptional regulationImmunology and Allergymedicine.symptomEuropean Journal of Immunology
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Genetic and environmental influences on the fibrinolytic system: a twin study.

2004

SummaryThe determination of heritability is a key issue to assess the predictive power of polymorphisms for disease in clinical studies. The aim of this study was to determine the heritability of proteins and activation markers of the fibrinolytic system in a large cohort of healthy twins. Heritability was calculated as 0.76 for thrombin activatable fibrinolysis inhibitor (TAFI), 0.44 for plasminogen activator inhibitor-1 (PAI-1), and 0.43 for tissue plasminogen activator. No significant genetic influence was observed for α2-antiplasmin-plasmin-complex and D-dimer. Heritability explained by single gene polymorphisms was 25.2% for TAFI 505G>A, 31.5% for 1542C>G, and 50.0% for combinati…

Malemedicine.medical_specialtyCarboxypeptidase B2GenotypeArteriosclerosismedicine.medical_treatmentBiologyEnvironmentTissue plasminogen activatorCohort StudiesFibrin Fibrinogen Degradation ProductsInternal medicineFibrinolysisPlasminogen Activator Inhibitor 1medicineDiseases in TwinsHumansFibrinolysinGeneGeneticsalpha-2-AntiplasminPolymorphism GeneticActivator (genetics)FibrinolysisHematologyTwins MonozygoticHeritabilityTwin studyEndocrinologyPhenotypeHaplotypesHemostasisTwin Studies as TopicFemalePlasminogen activatormedicine.drugThrombosis and haemostasis
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