PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27877174-3 2016 We report that the combination of the DNA methyltransferase inhibitor 5-azacytidine (5-Aza) and suboptimal T cell receptor (TCR) stimulation promoted CD4+CD25hFOXP3+ T cell induction from human CD4+CD25- T cells. Azacitidine 70-83 CD4 molecule Homo sapiens 150-153 27877174-4 2016 5-Aza treatment enhanced the expression of Treg cell signature genes, such as CD25, FOXP3, CTLA-4, and GITR, in CD4+CD25h cells. Azacitidine 0-5 CD4 molecule Homo sapiens 112-115 27877174-5 2016 Moreover, 5-Aza-treated CD4+CD25h T cells showed potent suppressive activity in a cell contact-dependent manner and reduced methylation in the Treg-specific demethylated region (TSDR) in the FOXP3 gene. Azacitidine 10-15 CD4 molecule Homo sapiens 24-27 27877174-6 2016 The analysis of cytokine production revealed that CD4+CD25- T cells with 5-Aza treatment produced comparable levels of interferon (IFN)-gamma and transforming growth factor (TGF)-beta, but less IL-10 and more IL-2, when compared to cells without 5-Aza treatment. Azacitidine 73-78 CD4 molecule Homo sapiens 50-53 27877174-6 2016 The analysis of cytokine production revealed that CD4+CD25- T cells with 5-Aza treatment produced comparable levels of interferon (IFN)-gamma and transforming growth factor (TGF)-beta, but less IL-10 and more IL-2, when compared to cells without 5-Aza treatment. Azacitidine 246-251 CD4 molecule Homo sapiens 50-53 27877174-7 2016 The increased IL-2 was indispensible to the enhanced FOXP3 expression in 5-Aza-treated CD4+CD25h cells. Azacitidine 73-78 CD4 molecule Homo sapiens 87-90 27877174-8 2016 Finally, 5-Aza-treated CD4+CD25h T cells could be expanded with IL-2 supplementation alone and maintained FOXP3 expression and suppressor function through the expansion. Azacitidine 9-14 CD4 molecule Homo sapiens 23-26 33570632-0 2021 Modulation of IL-6/STAT3 signaling axis in CD4+FOXP3- T cells represents a potential antitumor mechanism of azacitidine. Azacitidine 108-119 CD4 molecule Homo sapiens 43-46 33570632-3 2021 Azacitidine (AZA), the mainstay therapy for high-risk myelodysplastic syndromes (HR-MDS), affects CD4+ T-cell polarization and function, but whether this contributes to AZA efficacy is currently unknown. Azacitidine 0-11 CD4 molecule Homo sapiens 98-101 33570632-3 2021 Azacitidine (AZA), the mainstay therapy for high-risk myelodysplastic syndromes (HR-MDS), affects CD4+ T-cell polarization and function, but whether this contributes to AZA efficacy is currently unknown. Azacitidine 13-16 CD4 molecule Homo sapiens 98-101 33570632-4 2021 By using functional proteomic, transcriptomic, and mutational analyses in 73 HR-MDS patients undergoing AZA therapy, we demonstrate that responding patients exhibited a coordinated CD4+ T-cell immune response and downregulated the inflammatory cytokine signaling pathways in CD4+ T cells after AZA, in contrast to nonresponders who upregulated the same pathways. Azacitidine 104-107 CD4 molecule Homo sapiens 181-184 33570632-4 2021 By using functional proteomic, transcriptomic, and mutational analyses in 73 HR-MDS patients undergoing AZA therapy, we demonstrate that responding patients exhibited a coordinated CD4+ T-cell immune response and downregulated the inflammatory cytokine signaling pathways in CD4+ T cells after AZA, in contrast to nonresponders who upregulated the same pathways. Azacitidine 104-107 CD4 molecule Homo sapiens 275-278 33570632-4 2021 By using functional proteomic, transcriptomic, and mutational analyses in 73 HR-MDS patients undergoing AZA therapy, we demonstrate that responding patients exhibited a coordinated CD4+ T-cell immune response and downregulated the inflammatory cytokine signaling pathways in CD4+ T cells after AZA, in contrast to nonresponders who upregulated the same pathways. Azacitidine 294-297 CD4 molecule Homo sapiens 181-184 33570632-4 2021 By using functional proteomic, transcriptomic, and mutational analyses in 73 HR-MDS patients undergoing AZA therapy, we demonstrate that responding patients exhibited a coordinated CD4+ T-cell immune response and downregulated the inflammatory cytokine signaling pathways in CD4+ T cells after AZA, in contrast to nonresponders who upregulated the same pathways. Azacitidine 294-297 CD4 molecule Homo sapiens 275-278 33570632-5 2021 We further observed an AZA-mediated downregulation of intereukin-6 (IL-6)-induced STAT3 phosphorylation in CD4+FOXP3- conventional T cells (Tcons) that correlated independently with better response and survival, whereas it was also not associated with the mutation number and profile of the patients. Azacitidine 23-26 CD4 molecule Homo sapiens 107-110 33570632-6 2021 The AZA-induced downregulation of IL-6/STAT3 axis in Tcons restored the STAT signaling architecture in CD4+ T-cell subsets, whereas STAT signaling networks remained disorganized in patients who upregulated IL-6/STAT3 activity in Tcons. Azacitidine 4-7 CD4 molecule Homo sapiens 103-106 33570632-7 2021 Given the pivotal role of CD4+ T cells in adaptive immunity, our findings suggest that the downregulation of the IL-6/STAT3 pathway in Tcons potentially constitutes a previously unrecognized immune-mediated mechanism of action of AZA and sets the scene for developing rational strategies of AZA combinations with IL-6/STAT3 axis inhibitors. Azacitidine 230-233 CD4 molecule Homo sapiens 26-29 27877174-3 2016 We report that the combination of the DNA methyltransferase inhibitor 5-azacytidine (5-Aza) and suboptimal T cell receptor (TCR) stimulation promoted CD4+CD25hFOXP3+ T cell induction from human CD4+CD25- T cells. Azacitidine 70-83 CD4 molecule Homo sapiens 194-197 27877174-3 2016 We report that the combination of the DNA methyltransferase inhibitor 5-azacytidine (5-Aza) and suboptimal T cell receptor (TCR) stimulation promoted CD4+CD25hFOXP3+ T cell induction from human CD4+CD25- T cells. Azacitidine 85-90 CD4 molecule Homo sapiens 150-153 27877174-3 2016 We report that the combination of the DNA methyltransferase inhibitor 5-azacytidine (5-Aza) and suboptimal T cell receptor (TCR) stimulation promoted CD4+CD25hFOXP3+ T cell induction from human CD4+CD25- T cells. Azacitidine 85-90 CD4 molecule Homo sapiens 194-197 22503132-0 2012 Azacitidine differentially affects CD4(pos) T-cell polarization in vitro and in vivo in high risk myelodysplastic syndromes. Azacitidine 0-11 CD4 molecule Homo sapiens 35-38 23242597-9 2013 The in vitro addition of 5-azacytidine to CD4(+) T cells reduced the proliferative capacity of regulatory T cells (P=0.03). Azacitidine 25-38 CD4 molecule Homo sapiens 42-45 23242597-13 2013 Our data suggest that 5-azacytidine has profound effects on CD4(+) T cells, which correlate with disease status after treatment. Azacitidine 22-35 CD4 molecule Homo sapiens 60-63 25414732-14 2014 Treatment of CD4(+) T cells with 5-azacytidine (5-azaC) decreased CD11a promoter methylation and caused CD11a overexpression. Azacitidine 33-46 CD4 molecule Homo sapiens 13-16 25414732-14 2014 Treatment of CD4(+) T cells with 5-azacytidine (5-azaC) decreased CD11a promoter methylation and caused CD11a overexpression. Azacitidine 48-54 CD4 molecule Homo sapiens 13-16 25414732-15 2014 SSc CD4(+) T cells and 5-azaC-treated CD4(+) T cells showed increased proliferation of CD4(+) T cells, increased production of IgG by co-cultured B cells, and induced expression of COL1A2 mRNA by co-cultured fibroblasts. Azacitidine 23-29 CD4 molecule Homo sapiens 38-41 25414732-15 2014 SSc CD4(+) T cells and 5-azaC-treated CD4(+) T cells showed increased proliferation of CD4(+) T cells, increased production of IgG by co-cultured B cells, and induced expression of COL1A2 mRNA by co-cultured fibroblasts. Azacitidine 23-29 CD4 molecule Homo sapiens 38-41 22503132-1 2012 CD4(pos) T-cell subsets play a role in myelodysplastic syndromes (MDS) pathogenesis and may be affected upon 5-azacitidine (Aza) treatment. Azacitidine 109-122 CD4 molecule Homo sapiens 0-3 22503132-1 2012 CD4(pos) T-cell subsets play a role in myelodysplastic syndromes (MDS) pathogenesis and may be affected upon 5-azacitidine (Aza) treatment. Azacitidine 124-127 CD4 molecule Homo sapiens 0-3 22503132-4 2012 The overall number of T(H)17 was reduced both in vitro (p < 0.03) and in vivo (p < 0.006), indicating that Aza directly affects CD4(pos) polarization during activation in vitro. Azacitidine 113-116 CD4 molecule Homo sapiens 134-137 1692774-1 1990 The DNA methylation inhibitor 5-azacytidine induces autoreactivity in cloned CD4+ T cells, but the functional consequences of this response are unknown. Azacitidine 30-43 CD4 molecule Homo sapiens 77-80 1692774-2 1990 We now report that CD4+ T cells treated with 5-azacytidine respond to autologous antigen-presenting cells and induce autologous B cell differentiation without exogenous antigen or mitogen. Azacitidine 45-58 CD4 molecule Homo sapiens 19-22 34555853-4 2021 In this study, we leveraged a multiplexed immune assay to assess the functional states of CD4+ and CD8+ cells at a single-cell level in pretherapy bone marrows in 16 patients with R/R AML treated with azacitidine/nivolumab. Azacitidine 201-212 CD4 molecule Homo sapiens 90-93 17947713-8 2007 5-Azacytidine, a DNA methyltransferase inhibitor, demethylated CD40LG and doubled its expression on CD4(+) T cells from women but not men, while increasing TNFSF7 expression equally between sexes. Azacitidine 0-13 CD4 molecule Homo sapiens 63-66 17213580-8 2006 RESULTS: The perforin mRNA and protein in the CD4(+) and CD8(+) subsets treated with 5-azaC were significantly higher than those in the untreated subsets (P<0.05). Azacitidine 85-91 CD4 molecule Homo sapiens 46-49 17213580-10 2006 CONCLUSION: The mRNA and protein expression of perforin significantly increases in the CD4(+) and CD8(+) T cells treated with 5-azaC,which is associated with DNA hypomethylation of perforin promoter in T cells. Azacitidine 126-132 CD4 molecule Homo sapiens 87-90 34906298-6 2021 The changes of Th17 cell proportion and IL-17 expression were observed after adding methylation inhibitor 5-Aza-2"-deoxycytidine (5-Aza-dC) to CD4+ T cells. Azacitidine 130-135 CD4 molecule Homo sapiens 143-146 34906298-12 2021 After the addition of 5-Aza-dC in CD4+ T cells, the expression of miR-146a-3p was increased and the expression of IL-17 mRNA was decreased, and in the supernatant, the level of IL-17 was decreased and the proportion of Th17 cells was significantly reduced. Azacitidine 22-27 CD4 molecule Homo sapiens 34-37