scholarly journals Inflammatory Gene Expression Profile and Defective Interferon‐γ and Granzyme K in Natural Killer Cells From Systemic Juvenile Idiopathic Arthritis Patients

2016 ◽  
Vol 69 (1) ◽  
pp. 213-224 ◽  
Author(s):  
Karen Put ◽  
Jessica Vandenhaute ◽  
Anneleen Avau ◽  
Annemarie van Nieuwenhuijze ◽  
Ellen Brisse ◽  
...  
Keyword(s):  
Gene Expression ◽  
Juvenile Idiopathic Arthritis ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Systemic Juvenile Idiopathic Arthritis ◽  
Interferon Γ ◽  
Killer Cells ◽  
Inflammatory Gene Expression

scholarly journals Impact of Zygosity in Bimodal Phenotype Distributions

2016 ◽  
Author(s):  
Thomas Holst-Hansen ◽  
Elena Abad ◽  
Aura Muntasell ◽  
Miguel López-Botet ◽  
Mogens H. Jensen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Expression Profile ◽  
Positive Feedback ◽  
Expression Profiles ◽  
Receptor Protein ◽  
Killer Cells ◽  
Regulatory Circuit ◽  
The Relationship

AbstractAllele number, or zygosity, is a clear determinant of gene expression in diploid cells. But the relationship between the number of copies of a gene and its expression can be hard to anticipate, especially when the gene in question is embedded in a regulatory circuit that contains feedbacks. Here we study this question making use of the natural genetic variability of human populations, which allows us to compare the expression profiles of a receptor protein in natural killer cells between donors infected with human cytomegalovirus (HCMV) with one or two copies of the allele. Crucially, the distribution of gene expression in many of the donors is bimodal, indicative of the presence of a positive feedback somewhere in the regulatory environment of the gene. Three separate gene-circuit models differing in the location of the positive feedback with respect to the gene can all reproduce well the homozygous data. However, when the resulting fitted models are applied to the hemizygous donors, only one model (the one with the positive feedback located at the level of gene transcription) reproduces the experimentally observed gene-expression profile. In that way, our work shows that zygosity can help us relate structure and function of gene regulatory networks.Author SummaryNearly all mammalian cells, including human cells, have two copies of each chromosome, and thus possess two potentially different copies of each gene (which might be in some cases non-functional or even absent). Naïively one might expect that two identical copies of the gene would lead to the protein being expressed at twice the rate, but many factors can alter this simple calculation. One of these factors is the existence of feedback mechanisms affecting in one way or another the regulatory circuit in which our gene of interest is embedded. Here we study the relationship between the number of gene copies and the expression of a receptor protein that plays a crucial role in the recognition of pathogens by natural killer cells, which are important elements of the innate immune system. Experimental data of virus-infected donors reveals a bimodal expression profile of this receptor, typical of a positive feedback, and a clear difference between donors with one or two copies of the gene. Mathematical modeling allows us to find the likely location of the feedback loop within the gene’s regulatory circuit, by requiring the correct model to reproduce the expression profiles of both types of donors.

scholarly journals Natural Killer Cells Are Characterized by the Concomitantly Increased Interferon-γ and Cytotoxicity in Acute Resolved Hepatitis B Patients

PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e49135 ◽  
Author(s):  
Juanjuan Zhao ◽  
Yonggang Li ◽  
Lei Jin ◽  
Shuye Zhang ◽  
Rong Fan ◽  
...  
Keyword(s):  
Natural Killer Cells ◽  
Hepatitis B ◽  
Natural Killer ◽  
Interferon Γ ◽  
Killer Cells

scholarly journals Glucocorticoid receptor expression on circulating leukocytes differs between healthy male and female adults

2017 ◽  
Vol 1 (2) ◽  
pp. 108-114 ◽  
Author(s):  
Kim D. Lu ◽  
Shlomit Radom-Aizik ◽  
Fadia Haddad ◽  
Frank Zaldivar ◽  
Monica Kraft ◽  
...  
Keyword(s):  
Gene Expression ◽  
Flow Cytometry ◽  
Sexual Dimorphism ◽  
Natural Killer Cells ◽  
Glucocorticoid Receptor ◽  
Natural Killer ◽  
Peripheral Blood ◽  
Healthy Adults ◽  
Peripheral Blood Mononuclear ◽  
Killer Cells

IntroductionThe glucocorticoid receptor (GR) is a key receptor involved in inflammatory responses and is influenced by sex steroids. This study measured GR expression on circulating leukocyte subtypes in males and females.MethodsA total of 23 healthy adults (12 female) participated in this study. GR expression was measured in leukocyte subtypes using flow cytometry. Peripheral blood mononuclear cell (PBMC) gene expression of GR (NR3C1), GR β, TGF-β1 and 2, and glucocorticoid-induced leucine zipper (GILZ) were determined by real-time polymerase chain reaction.ResultsLeukocyte GR was lower in females, particularly in granulocytes, natural killer cells, and peripheral blood mononuclear cells (p≤0.01). GR protein expression was different across leukocyte subtypes, with higher expression in eosinophils compared with granulocytes, T lymphocytes, and natural killer cells (p<0.05). There was higher gene expression of GR β in males (p=0.03).ConclusionsThis is the first study to identify sexual dimorphism in GR expression in healthy adults using flow cytometry. These results may begin to explain the sexual dimorphism seen in many diseases and sex differences in glucocorticoid responsiveness.

scholarly journals Interferon-γ and Granulocyte/Monocyte Colony-stimulating Factor Production by Natural Killer Cells Involves Different Signaling Pathways and the Adaptor Stimulator of Interferon Genes (STING)

2013 ◽  
Vol 288 (15) ◽  
pp. 10715-10721 ◽  
Author(s):  
Fernando Souza-Fonseca-Guimaraes ◽  
Marianna Parlato ◽  
Rosane B. de Oliveira ◽  
Douglas Golenbock ◽  
Katherine Fitzgerald ◽  
...  
Keyword(s):  
Natural Killer Cells ◽  
Signaling Pathways ◽  
Natural Killer ◽  
Interferon Γ ◽  
Colony Stimulating Factor ◽  
Killer Cells ◽  
Factor Production ◽  
Stimulating Factor
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