Viewing affirmative mentions of gene expression of FOXP3 (H. sapiens) in T cells

Full-text article links are indicated by after the article reference.

Document Target Regulator Anatomy Sentence
Zhang et al. (2009)Foxp3T cellsRECENT FINDINGS: Recent findings have included identification of the signals that drive naive T lymphocytes to express Foxp3 in the thymus and the signals peripherally that induce non-Foxp3 expressing T cells to express FOXP3.
Yamamoto et al. (2008)FOXP3T cellsStudies of FOXP3 expression have thus far focused on T cells, including both normal and malignant T cells.
Ebert et al. (2008)FoxP3T-cellUntil recently, FoxP3 expression was thought to be restricted to the T-cell lineage.
Allan et al. (2007)FOXP3T cellThus expression of FOXP3 is a normal consequence of CD4(+) T cell activation and, in humans, it can no longer be used as an exclusive marker of nTregs.
Janson et al. (2008)FOXP3T cellsFurthermore, stimulated CD4(+)CD25(lo) T cells transiently expressed FOXP3 but remained partially methylated, suggesting promoter methylation as a mechanism for regulation of stable FOXP3 expression and Treg commitment.
Gavin et al. (2006)FOXP3T cellsInterestingly, one patient bearing a FOXP3 mutation enabling expression of stable FOXP3(mut) protein exhibited FOXP3(mut)-expressing cells among a subset of highly activated CD4+ T cells.
Baron et al. (2007)FOXP3T cellsImportantly, activated conventional CD4(+) T cells and TGF-beta-treated cells displayed no FOXP3 DNA demethylation despite expression of FOXP3, whereas subsets of Treg stable even upon extended in vitro expansion remained demethylated.
Hautz et al. (2009)Foxp3T-lymphocyteTo better define the characteristics of infiltrating cells, biopsies from human hand transplants have been investigated for expression of Foxp3 and indoleamine 2,3-dioxygenase (IDO), a key regulatory enzyme to induce T-lymphocyte unresponsiveness.
Broady et al. (2009)FOXP3T cellsATG-induced expression of FOXP3 in human CD4(+) T cells in vitro is associated with T-cell activation and not the induction of FOXP3(+) T regulatory cells.
Broady et al. (2009)FOXP3T cellsWe and others, however, have shown that FOXP3 is also expressed in activated T cells.
Broady et al. (2009)FOXP3T cellsWe found that exposure of peripheral blood mononuclear cells (PBMCs) or conventional T cells to rATG resulted in induction of transient rather than stable expression of CD25 and FOXP3.
Kim et al. (2007)FOXP3T cellsIn contrast to conversion of murine naive T cells to Tregs by transduction of Foxp3, it is controversial whether ectopic expression of FOXP3 in human CD4(+) T cells is sufficient for acquisition of suppressive activity.
Kim et al. (2007)FOXP3T cellsOur study demonstrates that enforced expression of FOXP3 confers Treg-like properties on Jurkat-T cells, which can be a convenient and efficient Treg-like cell model for further study to identify Treg cell surface markers and target genes regulated by FOXP3.
Grant et al. (2006)Foxp3T cellsOverexpression of Foxp3 in HEK 293T and purified CD4+ T cells resulted in a dose-dependent and time-dependent decrease in basal levels of nuclear factor-kappaB (NF-kappaB) activation.
Grant et al. (2006)Foxp3T cellsFinally, comparison of the percent Foxp3+CD4+CD25+ T cells to the HTLV-I proviral load in HTLV-I-infected asymptomatic carriers and patients with HTLV-I-associated myelopathy/tropical spastic paraparesis suggested that high Foxp3 expression is associated with low proviral load and absence of disease.
Du et al. (2008)FOXP3T cellsInterestingly, expression of RORalpha in T cells leads to the expression of genes that define Th17 cells, and the expression of each of these gene was inhibited by coexpression of full-length, but not DeltaEx2, FOXP3.
Wang et al. (2007)FOXP3T cellsTransient expression of FOXP3 in human activated nonregulatory CD4+ T cells.
Wang et al. (2007)FOXP3T cellsDespite the strong association between FOXP3 expression and regulatory function in fresh human T cells, little is known about the dynamics of endogenous FOXP3 expression and its relation to the suppressive function in activated human T cells.
Wang et al. (2007)FOXP3T cellHere, we addressed the dynamics of FOXP3 expression during human CD4+ T cell activation by plate-bound anti-CD3 Ab as well as the relationship between its expression and regulatory function at the single-cell level.
Wang et al. (2007)FOXP3T cellsOur data show that FOXP3 is expressed in a high percentage of activated T cells after in vitro stimulation of human CD4+ CD25- cells.
Wang et al. (2007)FOXP3T cellsFOXP3 expression is strongly associated with hyporesponsiveness of activated T cells, but is not directly correlated with their suppressive capabilities, as we demonstrate that it is also expressed in activated nonsuppressive T cells.
Wang et al. (2007)FOXP3T cellHowever, in this nonsuppressive T cell population, FOXP3 expression is transient, while it is stably expressed in activated T cells that do display suppressive function, and in natural CD4+ CD25++ T(reg) cells.
Pillai et al. (2007)FOXP3T-cellsOur results show that, in humans, FOXP3 expression and T(reg) functionality are not exclusive features of a stable or unique lineage of T-cells but may also be a transient state attained by almost all T-cells.
Kmieciak et al. (2009)Foxp3T cellsEctopic expression of Foxp3 was shown to be sufficient to activate a program of suppressor function in peripheral murine CD4+ T cells [2].
Kmieciak et al. (2009)Foxp3T cellsActivation of T cells induces expression of CD25 and Foxp3 associated with effector and memory phenotype differentiation
Kmieciak et al. (2009)FoxP3T cellsExpression of FoxP3 was also determined on freshly isolated T cells on day 0.
Kmieciak et al. (2009)Foxp3T cellsThe B/I activation, however, induced Foxp3 and CD25 expression in CD4+ and CD8+ T cells (Fig. 1A, middle panel).
Kmieciak et al. (2009)Foxp3T cellsThese results suggest that activation-induced expression of Foxp3 in CD4+CD25+ T cells is more stable than that in CD8+CD25+ T cells.
Kmieciak et al. (2009)FoxP3T cellsUpon B/I activation, CD4+ T cells showed a 6-fold increases of FoxP3 expression in CD44+, CD62L+ phenotypes (CD44+: 2.6% to 15%; CD62L+: 2% to 12%).
Abe et al. (2008)Foxp3T-cellFoxp3 expression on normal and leukemic CD4+CD25+ T cells implicated in human T-cell leukemia virus type-1 is inconsistent with Treg cells.
Abe et al. (2008)Foxp3T cellsWe describe here different features in Foxp3 expression profile between normal and leukemic CD4(+)CD25(+) T cells, using peripheral blood samples from healthy controls (HCs), human T-cell leukemia virus type-1 (HTLV-1)-infected asymptomatic carriers (ACs), patients with adult T-cell leukemia (ATL), and various hematopoietic cell lines.
Abe et al. (2008)Foxp3T cellsThe majority of CD4(+)CD25(+) T cells in HCs were positive for Foxp3, but not all CD4(+)CD25(+) T cells in ACs were positive, indicating that Foxp3 expression is not always linked to CD25 expression in normal T cells.
Abe et al. (2008)Foxp3T cellsLeukemic (ATL) T cells constitutively expressing CD25 were characteristic of heterogeneous Foxp3 expression, such as intra- and inter-case heterogeneity in intensity, inconsistency with CD25 expression, and a discrepancy in the mRNA and its protein expression.
Abe et al. (2008)Foxp3T cellsConclusively, Foxp3 in normal T cells, but not mRNA, is basically potent at discriminating a subset of Treg cells from CD25(+) T-cell populations, whereas the modulation of Foxp3 expression in leukemic T cells could be implicated in oncogenesis and has a potentially useful clinical role.
Yuan et al. (2010)Foxp3T-cellElevated expression of Foxp3 in tumor-infiltrating Treg cells suppresses T-cell proliferation and contributes to gastric cancer progression in a COX-2-dependent manner.
Morgan et al. (2005)FOXP3T-cellIn order to determine whether FOXP3 expression is confined to CD4(+)CD25(+) T cells with a regulatory phenotype, we analyzed several well-defined T-cell clones and lines with various specificities.
Radulovic et al. (2008)Foxp3T cellsDual-immunofluorescence microscopy was used to enumerate and colocalize Foxp3 expression to CD4(+) and CD25(+) T cells in the nasal mucosa.
Oswald-Richter et al. (2004)FoxP3T-cellsBecause Treg cells are present in very few numbers and are difficult to expand in vitro, we genetically modified conventional human T-cells to generate Treg cells in vitro by ectopic expression of FoxP3, a transcription factor associated with reprogramming T-cells into a Treg subset.
Oswald-Richter et al. (2004)FoxP3T-cellsOverexpression of FoxP3 in nave human CD4+ T-cells recapitulated the hyporesponsiveness and suppressive function of naturally occurring Treg cells.
Oswald-Richter et al. (2004)FOXP3T-cellsIn addition, expression of FOXP3 in conventional T-cells either in transgenic mice or by retroviral transduction is sufficient to confer a Treg cell phenotype (Fontenot et al. 2003; Hori et al. 2003; Khattri et al. 2003).
Oswald-Richter et al. (2004)FoxP3T-cellsEctopic expression of FoxP3 in conventional human T-cells genetically reprogrammed them into a Treg phenotype and enhanced their susceptibility to HIV infection.
Oswald-Richter et al. (2004)FoxP3T-cellsTherefore we hypothesized that ectopic expression of FoxP3 in nave T-cells could facilitate the generation of large numbers of human Treg cells.
Oswald-Richter et al. (2004)FoxP3T-cellsNave T-cells ectopically expressing FoxP3 displayed higher levels of CD25, GITR (Figure 5A), and CCR4 (Figure 5B) as compared to control transduced T-cells.
Oswald-Richter et al. (2004)FoxP3T-cellsWe conclude that ectopic expression of FoxP3 in nave human T-cells recapitulates key phenotypic and functional features of naturally occurring Treg cells.
Oswald-Richter et al. (2004)FoxP3T-cellsThese findings demonstrate that the expression of FoxP3 renders CD4+ primary T-cells more susceptible to HIV infection.
Oswald-Richter et al. (2004)FoxP3T-cellIn order to normalize for experimental variability, FoxP3 expression of the CD4+CD25hi cells was normalized to GAPDH levels from the same samples and compared to the nave T-cell subset isolated from the same donor.
Oswald-Richter et al. (2004)FoxP3T-cellsWe found that within HIV-negative subjects there was on average a 49-fold higher level of expression of FoxP3 in CD4+CD25hi cells as compared to nave T-cells (Figure 9A).
Oswald-Richter et al. (2004)FoxP3T-cellIndeed, we found that in a subset of HIV-infected subjects, the CD4+CD25hi T-cell subset had greatly reduced FoxP3 expression, suggesting that these cells represent recently activated T-cells rather then Treg cells.
Oswald-Richter et al. (2004)FoxP3T-cellsIn summary, our results indicate that both naturally occurring and genetically reprogrammed Treg cells are susceptible to HIV infection and that ectopic FoxP3 expression greatly increases the susceptibility of T-cells to HIV infection.
Roncador et al. (2005)FOXP3T cellsFlow-cytometric analysis showed that FOXP3 was expressed by the majority of CD4(+)CD25(high) T cells in peripheral blood.
Roncador et al. (2005)FOXP3T cellAlthough FOXP3 expression was primarily restricted to CD4(+)CD25(+) cells, it was induced following activation of both CD4(+) and CD8(+) T cell clones.
Janson et al. (2008)FOXP3T cellsOur data strongly suggests that the transient FOXP3 expression by activated T cells, observed by us and others, is a consequence of the methylation status at the FOXP3 promoter region.
Janson et al. (2008)FOXP3T cellsThe transient expression of FOXP3 in activated T cells has been proposed as a mechanism of attenuating the activated state in these cells, but whether activated transient FOXP3 expressing T cells also have the capacity to suppress neighbouring cells is an unresolved matter [13][15], [17].
Janson et al. (2008)FOXP3T cellIn order to investigate whether the transient expression of FOXP3 during T cell activation was associated with FOXP3 promoter demethylation, we analyzed male CD4+CD25lo cells with respect to their methylation status during stimulation (Figure 6A).
Janson et al. (2008)FOXP3T cellsThese results confirm that FOXP3 expression occurs in CD4+CD25lo T cells upon stimulation, and thus is not solely limited to the Treg population in humans.
Janson et al. (2008)FOXP3T cellsTherefore, we stimulated CD4+CD25lo T cells with anti-CD3/CD28 Dynabeads for 48 hours and monitored the expression of FOXP3 and CD25 up to day 16 of culture (Figure 5A).
Janson et al. (2008)FOXP3T cellsJust as CD25, FOXP3 is transiently upregulated in human CD4+CD25lo T cells upon activation [10][15] and although this FOXP3 expression is associated with hyporesponsiveness and decreased cytokine production, results regarding the suppressive ability of these cells differ [14], [16], [17].
Janson et al. (2008)Foxp3T cellsAlthough transient expression of Foxp3 has been observed in murine activated T cells [9], Foxp3 is not only considered a specific marker for the Treg population but it is also required and sufficient for Treg development in the murine setting [1], [3].
Ahmadzadeh et al. (2007)FOXP3T cellsIL-2 and IL-15 each mediate de novo induction of FOXP3 expression in human tumor antigen-specific CD8 T cells.
Ahmadzadeh et al. (2007)FOXP3T cellsAlthough FOXP3 is primarily expressed by regulatory CD4 T cells (Treg) in vivo, polyclonal activation of human CD8 T cells can result in the expression of FOXP3 in a fraction of CD8 T cells.
Ahmadzadeh et al. (2007)FOXP3T cellsHere, we demonstrate that interleukin-2 (IL-2) induces FOXP3 expression in OKT3-stimulated or antigen-stimulated CD8 T cells, indicating that FOXP3 expression is neither limited to a unique subset of CD8 T cells nor dependent on the mode of T-cell receptor stimulation.
Ahmadzadeh et al. (2007)FOXP3T cellsIn the absence of IL-2, antigen stimulation resulted in T-cell activation and acquisition of effector function without induction of FOXP3, indicating that acquisition of effector function is independent of induction of FOXP3 expression in CD8 T cells.
Ahmadzadeh et al. (2007)FOXP3T cellsThese findings indicate that induction of FOXP3 is intrinsic to CD8 T cells that are activated in the presence of IL-2 or IL-15, and in vitro-induced expression of FOXP3 cannot be simply interpreted as an indicator of Treg activity or activation marker.
de Zoeten et al. (2009)Foxp3T cellsWe show, using retroviral expression of Foxp3 in CD4(+) T cells, that Foxp3 is cleaved at both the N- and C-terminal RXXR sites and that mutagenesis of the RXXR motif prevents cleavage.
Rouas et al. (2009)FOXP3T cellsUsing lentiviral transduction of fresh cord blood T cells, we demonstrated that miR-31 and miR-21 had an effect on FOXP3 expression levels.
Suchard et al. (2010)FOXP3T cellsWe found a significantly elevated percentage of FOXP3 expressing CD4+ T cells in HIV infected patients, particularly in those with lower CD4 counts.
Suchard et al. (2010)FOXP3T cellWe explored the mechanism of FOXP3 upregulation by assessing the ability of cultured cells from HIV positive and negative patients to maintain FOXP3 expression in unstimulated conditions and following T cell receptor stimulation.
Suchard et al. (2010)FOXP3T cellWe sought to investigate FOXP3 expression after T cell receptor stimulation while maintaining a physiological ratio of Tregs to responder cells.
Suchard et al. (2010)FOXP3T cellFOXP3 expression dropped rapidly in unstimulated cell culture but was restored by T cell receptor stimulation.
Suchard et al. (2010)FOXP3T cellsThis suggests that the high FOXP3 expression in HIV infected patients is likely due to FOXP3 upregulation by individual CD4+ T cells following antigenic or other stimulation.
Suchard et al. (2010)FOXP3T cellCD4+ T cell FOXP3 expression is negatively correlated with CD4+ T cell count and positively correlated with viral load
Suchard et al. (2010)FOXP3T cellsAs FOXP3 expression may be affected by the degree of immunodeficiency, we analysed the relationship between the CD4+T cell count and the percentage of CD4+T cells expressing FOXP3.
Suchard et al. (2010)FOXP3T cellsFOXP3 expression in CD8+ T cells has been described [9], [52], [56], [57], [61], [62], [63], [64], as have other subsets of FOXP3?
Suchard et al. (2010)FOXP3T cellsHIV infected individuals are known to exhibit high levels of T cell activation and debate reigns as to whether FOXP3 is expressed by activated T cells that do not possess suppressive functions [52], [56], [58].
Suchard et al. (2010)FOXP3T cellWe explored whether this was due to increased CD4+ T cell proliferation or increased FOXP3 expression in cells which had proliferated.
Suchard et al. (2010)FOXP3T cellUsing dual labelling with CFSE and FOXP3 we found that total CD4+ T cell proliferation was lower in the HIV group than in the control group, and the percentage of proliferated cells that expressed FOXP3 was similar in both groups.
Suchard et al. (2010)FOXP3T cellThus the mechanism by which FOXP3 expression was upregulated in vitro in response to anti-CD3 stimulation is not likely to be due to CD4+ T cell proliferation.
Suchard et al. (2010)FOXP3T cellsTogether, these findings suggest that elevated FOXP3 percentages in HIV infected individuals is due to upregulation of FOXP3 expression in individual CD4+ T cells in HIV, likely due to antigenic or other stimulation.
Suchard et al. (2010)FOXP3T cellWe suggest that FOXP3 expression in the CD4+ T cell subset may prove a more accurate prognostic tool to monitor disease progression and response to antiretroviral therapy.
Suchard et al. (2010)FOXP3T cellsIn conclusion, we have shown that HIV infected individuals had significantly higher percentages of CD4+ T cells positive for FOXP3 than HIV uninfected individuals and that this is likely due to upregulation of FOXP3 expression by CD4+ T cells.
Suchard et al. (2010)FOXP3T cellsFOXP3 expression as a percentage of CD4+ T cells correlated positively with viral load and negatively with CD4 count, with a marked elevation in FOXP3 percentage in patients with CD4 counts below 200 cells/l.
Suchard et al. (2010)FOXP3T cellsThe basis of the increased FOXP3 expression appears to be upregulation of FOXP3 expression by individual CD4+ T cells following T cell receptor stimulation.
Suchard et al. (2010)FOXP3T cellFOXP3 expression as a percentage of the CD4+ T cell population is a potential prognostic marker of disease progression.
Allan et al. (2005)FOXP3T cellsSurprisingly, although ectopic expression of FOXP3 in human CD4+ T cells resulted in induction of hyporesponsiveness and suppression of IL-2 production, it did not lead to acquisition of significant suppressor activity in vitro.
Scholzen et al. (2009)Foxp3T cellsWe found that iRBCs, at concentrations typically found during mild/uncomplicated human malaria infection [12],[13], dose-dependently induce two populations of CD4+CD25hi T cells, which express Foxp3 at high or intermediate levels and have distinct cell-contact and cytokine requirements for their induction.
Scholzen et al. (2009)Foxp3T cellsSpecific Foxp3 expression in the induced CD25hi CD4 T cells compared to CD4+CD25?
Scholzen et al. (2009)Foxp3T cellsFoxp3 expression in CD4 T cells was not induced when purified T cells as opposed to whole PBMCs were co-cultured with iRBCs, demonstrating that induction of Foxp3+ CD4 T cells is not due to a direct interaction of T cells with iRBCs but dependent on other cells present in the co-culture system (Figure 5A).
Scholzen et al. (2009)Foxp3T cellsMonocytes further required direct contact with T cells to induce both CD25hiFoxp3hi and CD25hiFoxp3int CD4 T cells, as separation of T cells and monocytes through a transwell abrogated induction of Foxp3 expression (P<0.001, one-way ANOVA with Neuman-Keuls' post-test) (Figure 5B).
Scholzen et al. (2009)Foxp3T cellsIn this study, we set out to determine whether the above signals also govern the induction of Foxp3 expression in human CD4 T cells by malaria-infected RBCs in the absence of any other exogenous stimuli.
Scholzen et al. (2009)Foxp3T cellsmRNA were sufficient for iRBC-induced Foxp3 expression in purified T cells.
Scholzen et al. (2009)Foxp3T cellsThe induction of Foxp3 expression occurred in transwell-separated responder/bystander T cells solely responding to soluble factors without their direct interaction with monocytes.