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Epigenetic control of interferon-gamma expression in CD8 T cells.

de Araújo-Souza PS, Hanschke SC, Viola JP - J Immunol Res (2015)

Bottom Line: However, naïve CD8 T lymphocytes do not produce large amounts of IFN-γ, but after TCR stimulation there is a progressive acquisition of IFN-γ expression during differentiation into cytotoxic T lymphocytes (CTL) and memory cells, which are capable of producing high levels of this cytokine.Differential gene expression can be regulated from the selective action of transcriptional factors and also from epigenetic mechanisms, such as DNA CpG methylation or posttranslational histone modifications.This review will focus on the chromatin status of Ifng promoter in CD8 T cells and possible influences of epigenetic modifications in Ifng gene and conserved noncoding sequences (CNSs) in regulation of IFN-γ production by CD8 T lymphocytes.

View Article: PubMed Central - PubMed

Affiliation: Program of Cellular Biology, Brazilian National Cancer Institute (INCA), Rua André Cavalcanti 37, Centro, 20231-050 Rio de Janeiro, RJ, Brazil ; Department of Immunobiology, Biology Institute, Fluminense Federal University (UFF), Outeiro São João Batista s/n, Centro, 24020-141 Niterói, RJ, Brazil.

ABSTRACT
Interferon- (IFN-) γ is an essential cytokine for immunity against intracellular pathogens and cancer. IFN-γ expression by CD4 T lymphocytes is observed only after T helper (Th) 1 differentiation and there are several studies about the molecular mechanisms that control Ifng expression in these cells. However, naïve CD8 T lymphocytes do not produce large amounts of IFN-γ, but after TCR stimulation there is a progressive acquisition of IFN-γ expression during differentiation into cytotoxic T lymphocytes (CTL) and memory cells, which are capable of producing high levels of this cytokine. Differential gene expression can be regulated from the selective action of transcriptional factors and also from epigenetic mechanisms, such as DNA CpG methylation or posttranslational histone modifications. Recently it has been recognized that epigenetic modification is an integral part of CD8 lymphocyte differentiation. This review will focus on the chromatin status of Ifng promoter in CD8 T cells and possible influences of epigenetic modifications in Ifng gene and conserved noncoding sequences (CNSs) in regulation of IFN-γ production by CD8 T lymphocytes.

No MeSH data available.


Related in: MedlinePlus

Schematic view of mouse interferon-γ locus (Ifng). Exons are shown as black boxes. In detail, the relative positions of the CpG sites located at the Ifng promoter are indicated. The numbers correspond to their distance relative to the transcription start site (+1) of the Ifng.
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fig1: Schematic view of mouse interferon-γ locus (Ifng). Exons are shown as black boxes. In detail, the relative positions of the CpG sites located at the Ifng promoter are indicated. The numbers correspond to their distance relative to the transcription start site (+1) of the Ifng.

Mentions: The importance of CpG methylation for Ifng expression is supported by experiments of CD8 T cell cultures stimulated via TCR in the presence of 5-azacytidine (5-AZA), a drug that causes DNA demethylation upon proliferation. Upon AZA treatment, increased levels of this cytokine in culture supernatants were described [31], as well as an increment in the number of naïve cells able to produce IFN-γ when compared to control [32]. Several genomic regions could be involved in this regulation and a possible role of Ifng mouse promoter was particularly investigated. The ~600 pb region contains 10 CpG sites (Figure 1). Numeration of these sites varies among different publications, but here we will denominate it according to the initial transcription site from the RefSeq sequence identifier NM_008337.


Epigenetic control of interferon-gamma expression in CD8 T cells.

de Araújo-Souza PS, Hanschke SC, Viola JP - J Immunol Res (2015)

Schematic view of mouse interferon-γ locus (Ifng). Exons are shown as black boxes. In detail, the relative positions of the CpG sites located at the Ifng promoter are indicated. The numbers correspond to their distance relative to the transcription start site (+1) of the Ifng.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4418004&req=5

fig1: Schematic view of mouse interferon-γ locus (Ifng). Exons are shown as black boxes. In detail, the relative positions of the CpG sites located at the Ifng promoter are indicated. The numbers correspond to their distance relative to the transcription start site (+1) of the Ifng.
Mentions: The importance of CpG methylation for Ifng expression is supported by experiments of CD8 T cell cultures stimulated via TCR in the presence of 5-azacytidine (5-AZA), a drug that causes DNA demethylation upon proliferation. Upon AZA treatment, increased levels of this cytokine in culture supernatants were described [31], as well as an increment in the number of naïve cells able to produce IFN-γ when compared to control [32]. Several genomic regions could be involved in this regulation and a possible role of Ifng mouse promoter was particularly investigated. The ~600 pb region contains 10 CpG sites (Figure 1). Numeration of these sites varies among different publications, but here we will denominate it according to the initial transcription site from the RefSeq sequence identifier NM_008337.

Bottom Line: However, naïve CD8 T lymphocytes do not produce large amounts of IFN-γ, but after TCR stimulation there is a progressive acquisition of IFN-γ expression during differentiation into cytotoxic T lymphocytes (CTL) and memory cells, which are capable of producing high levels of this cytokine.Differential gene expression can be regulated from the selective action of transcriptional factors and also from epigenetic mechanisms, such as DNA CpG methylation or posttranslational histone modifications.This review will focus on the chromatin status of Ifng promoter in CD8 T cells and possible influences of epigenetic modifications in Ifng gene and conserved noncoding sequences (CNSs) in regulation of IFN-γ production by CD8 T lymphocytes.

View Article: PubMed Central - PubMed

Affiliation: Program of Cellular Biology, Brazilian National Cancer Institute (INCA), Rua André Cavalcanti 37, Centro, 20231-050 Rio de Janeiro, RJ, Brazil ; Department of Immunobiology, Biology Institute, Fluminense Federal University (UFF), Outeiro São João Batista s/n, Centro, 24020-141 Niterói, RJ, Brazil.

ABSTRACT
Interferon- (IFN-) γ is an essential cytokine for immunity against intracellular pathogens and cancer. IFN-γ expression by CD4 T lymphocytes is observed only after T helper (Th) 1 differentiation and there are several studies about the molecular mechanisms that control Ifng expression in these cells. However, naïve CD8 T lymphocytes do not produce large amounts of IFN-γ, but after TCR stimulation there is a progressive acquisition of IFN-γ expression during differentiation into cytotoxic T lymphocytes (CTL) and memory cells, which are capable of producing high levels of this cytokine. Differential gene expression can be regulated from the selective action of transcriptional factors and also from epigenetic mechanisms, such as DNA CpG methylation or posttranslational histone modifications. Recently it has been recognized that epigenetic modification is an integral part of CD8 lymphocyte differentiation. This review will focus on the chromatin status of Ifng promoter in CD8 T cells and possible influences of epigenetic modifications in Ifng gene and conserved noncoding sequences (CNSs) in regulation of IFN-γ production by CD8 T lymphocytes.

No MeSH data available.


Related in: MedlinePlus