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PMID |
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1 |
28939757
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PD-1 Blockade Promotes Epitope Spreading in Anticancer CD8+ T Cell Responses by Preventing Fratricidal Death of Subdominant Clones To Relieve Immunodomination.
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2 |
28939757
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The interactions between programmed death-1 (PD-1) and its ligands hamper tumor-specific CD8+ T cell (TCD8) responses, and PD-1-based "checkpoint inhibitors" have shown promise in certain cancers, thus revitalizing interest in immunotherapy.
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3 |
28939757
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We found that unlike other coinhibitory molecules (CTLA-4, LAG-3, TIM-3), PD-1 was highly expressed by subdominant TCD8, which correlated with their propensity to favorably respond to PD-1/PD-1 ligand-1 (PD-L1)-blocking Abs.
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4 |
28939757
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PD-1 blockade increased the size of subdominant TCD8 clones at the peak of their primary response, and it also sustained their presence, thus giving rise to an enlarged memory pool.
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5 |
28939757
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Further mechanistic studies utilizing peptide-pulsed dendritic cells, recombinant vaccinia viruses encoding full-length T Ag or epitope mingenes, and tumor cells expressing T Ag variants revealed that anti-PD-1 invigorates subdominant TCD8 responses by relieving their lysis-dependent suppression by immunodominant TCD8 To our knowledge, our work constitutes the first report that interfering with PD-1 signaling potentiates epitope spreading in tumor-specific responses, a finding with clear implications for cancer immunotherapy and vaccination.
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6 |
28442041
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Genes with altered expression in sheep SCNT placentas included cytotoxic T-lymphocyte-associated protein 4 (CTLA4), interleukin 2 receptor alpha (IL2RA), cluster of differentiation 28 (CD28), interferon gamma (IFNG), interleukin 6 (IL6), interleukin 10 (IL10), transforming growth factor beta 1 (TGFB1), tumor necrosis factor alpha (TNF-α), interleukin 1 alpha (IL1A) and chemokine (C-X-C motif) ligand 8 (CXCL8).
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7 |
28257599
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Immunosuppressive drugs affect interferon (IFN)-γ and programmed cell death 1 (PD-1) kinetics in patients with newly diagnosed autoimmune hepatitis.
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8 |
28257599
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Herein we investigate the in-vitro effects of prednisolone, 6-mercaptopurine, cyclosporin, tacrolimus, mycophenolic acid (MPA) and rapamycin, immunosuppressive drugs (ISDs) used in AIH treatment, on the expression of proinflammatory cytokines, co-inhibitory molecules and ability to proliferate of CD4+ CD25- cells, isolated from the peripheral blood of treatment-naive patients with AIH.
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9 |
28257599
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We note that in healthy subjects (HS) following polyclonal stimulation and in the absence of ISDs, the expression of interferon (IFN)-γ, interleukin (IL)-17 and tumour necrosis factor (TNF)-α by CD4 effectors peaks at 48 h and decreases at 96 h to reach baseline levels.
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10 |
28257599
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Levels of programmed cell death-1 (PD-1), T cell immunoglobulin and mucin domain-containing molecule-3 (TIM-3) and cytotoxic T lymphocyte antigen-4 (CTLA-4) increase over 96-h culture both in HS and AIH, although with faster kinetics in the latter.
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11 |
28257599
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Exposure to ISDs contains IFN-γ and PD-1 expression in AIH, where control over CD4+ CD25- cell proliferation is also noted upon exposure to MPA.
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12 |
28257599
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Treatment with tacrolimus and cyclosporin render CD4+ CD25- cells more susceptible to Treg control.
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13 |
28250252
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Association of IL10, IL4, IFNG, and CTLA4 Gene Polymorphisms with Efavirenz Hypersensitivity Reaction in Patients Infected with Human Immunodeficiency Virus.
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14 |
28250252
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Association of IL10, IL4, IFNG, and CTLA4 Gene Polymorphisms with Efavirenz Hypersensitivity Reaction in Patients Infected with Human Immunodeficiency Virus.
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15 |
28250252
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Association of IL10, IL4, IFNG, and CTLA4 Gene Polymorphisms with Efavirenz Hypersensitivity Reaction in Patients Infected with Human Immunodeficiency Virus.
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16 |
28250252
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We evaluated interleukin-10 (IL10) -592 C/A, IL4-589 C/T, interferon gamma (IFNG)+874 A/T, cytotoxic T-lymphocyte-associated antigen 4 (CTLA4)+49 A/G gene polymorphisms associated with efavirenz hypersensitivity reaction.
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17 |
28250252
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We evaluated interleukin-10 (IL10) -592 C/A, IL4-589 C/T, interferon gamma (IFNG)+874 A/T, cytotoxic T-lymphocyte-associated antigen 4 (CTLA4)+49 A/G gene polymorphisms associated with efavirenz hypersensitivity reaction.
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18 |
28250252
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We evaluated interleukin-10 (IL10) -592 C/A, IL4-589 C/T, interferon gamma (IFNG)+874 A/T, cytotoxic T-lymphocyte-associated antigen 4 (CTLA4)+49 A/G gene polymorphisms associated with efavirenz hypersensitivity reaction.
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19 |
28250252
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A significant inverse correlation was observed when comparing the CTLA4+49A/G and IL4 -589 C/T polymorphisms (r=-0.650, p=0.001); that is, the CTLA4 +49GG genotype, involved with the lowest capacity of inhibition, was inversely correlated IL4-589TT genotype, which induces high production of IL-4.
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20 |
28250252
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A significant inverse correlation was observed when comparing the CTLA4+49A/G and IL4 -589 C/T polymorphisms (r=-0.650, p=0.001); that is, the CTLA4 +49GG genotype, involved with the lowest capacity of inhibition, was inversely correlated IL4-589TT genotype, which induces high production of IL-4.
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21 |
28250252
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A significant inverse correlation was observed when comparing the CTLA4+49A/G and IL4 -589 C/T polymorphisms (r=-0.650, p=0.001); that is, the CTLA4 +49GG genotype, involved with the lowest capacity of inhibition, was inversely correlated IL4-589TT genotype, which induces high production of IL-4.
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22 |
27864228
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Mice bearing melanoma tumors that lacked one of these genes, IFNGR1, also had an impaired response to anti-CTLA-4 therapy and significantly reduced overall survival, compared with their counterparts whose tumors had intact IFNGR1.
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23 |
27668605
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Carriage frequencies of alleles and genotypes of polymorphic loci of inflammation genes (49A>G CTLA4, 41G>A and 87C>T PDE4D, -590C>T IL4, -308A>G TNF, 252G>A LTA, 874A>T IFNG, -509С>Т, 869T>C and 915G>C TGFB1) were determined in a sample of 200 patients diagnosed with ischemic stroke and in the control group similar in gender and age (146 individuals), all ethnic Russians.
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24 |
27443592
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There was a concomitant decrease in CTLA-4 expression on CD25(hi)Foxp3(+) Treg cells (p=0.0093) and PD-1 levels on CD8(+) T cells (p=0.0002).
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25 |
27443592
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There was a concomitant decrease in CTLA-4 expression on CD25(hi)Foxp3(+) Treg cells (p=0.0093) and PD-1 levels on CD8(+) T cells (p=0.0002).
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26 |
27443592
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Additionally, the frequency of anergic CTLA-4(+)CCR7(+) T cells decreased following vaccination.
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27 |
27443592
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Additionally, the frequency of anergic CTLA-4(+)CCR7(+) T cells decreased following vaccination.
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28 |
27139489
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This T cell chemokine facilitated the retention of antiviral CD4(+) T cells in the liver in a CXCR3-dependent manner.
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29 |
27139489
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Hepatic sequestrated antiviral CD4(+) T cells subsequently underwent local apoptotic elimination partially via cytotoxic T lymphocyte-associated protein 4 ligation.
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30 |
25219326
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Molecular landscape of T cell-mediated rejection in human kidney transplants: prominence of CTLA4 and PD ligands.
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31 |
25219326
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Molecular landscape of T cell-mediated rejection in human kidney transplants: prominence of CTLA4 and PD ligands.
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32 |
25219326
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Molecular landscape of T cell-mediated rejection in human kidney transplants: prominence of CTLA4 and PD ligands.
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33 |
25219326
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Molecular landscape of T cell-mediated rejection in human kidney transplants: prominence of CTLA4 and PD ligands.
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34 |
25219326
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CTLA4, CD28, IFNG), macrophages (e.g.
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35 |
25219326
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CTLA4, CD28, IFNG), macrophages (e.g.
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36 |
25219326
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CTLA4, CD28, IFNG), macrophages (e.g.
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37 |
25219326
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CTLA4, CD28, IFNG), macrophages (e.g.
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38 |
25219326
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PDL1, CD86, SLAMF8, ADAMDEC1), B cells (e.g.
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39 |
25219326
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PDL1, CD86, SLAMF8, ADAMDEC1), B cells (e.g.
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40 |
25219326
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PDL1, CD86, SLAMF8, ADAMDEC1), B cells (e.g.
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41 |
25219326
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PDL1, CD86, SLAMF8, ADAMDEC1), B cells (e.g.
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42 |
25219326
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CD72, BTLA) and IFNG-treated macrophages (e.g.
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43 |
25219326
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CD72, BTLA) and IFNG-treated macrophages (e.g.
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44 |
25219326
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CD72, BTLA) and IFNG-treated macrophages (e.g.
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45 |
25219326
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CD72, BTLA) and IFNG-treated macrophages (e.g.
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46 |
25219326
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ANKRD22, AIM2).
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47 |
25219326
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ANKRD22, AIM2).
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48 |
25219326
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ANKRD22, AIM2).
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49 |
25219326
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ANKRD22, AIM2).
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50 |
25219326
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In pathway analysis, the top pathways included T cell receptor signaling and CTLA4 costimulation.
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51 |
25219326
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In pathway analysis, the top pathways included T cell receptor signaling and CTLA4 costimulation.
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52 |
25219326
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In pathway analysis, the top pathways included T cell receptor signaling and CTLA4 costimulation.
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53 |
25219326
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In pathway analysis, the top pathways included T cell receptor signaling and CTLA4 costimulation.
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54 |
25219326
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The prominence of inhibitors like CTLA4 and PDL1 raises the possibility of active negative controls within the rejecting tissue.
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55 |
25219326
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The prominence of inhibitors like CTLA4 and PDL1 raises the possibility of active negative controls within the rejecting tissue.
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56 |
25219326
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The prominence of inhibitors like CTLA4 and PDL1 raises the possibility of active negative controls within the rejecting tissue.
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57 |
25219326
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The prominence of inhibitors like CTLA4 and PDL1 raises the possibility of active negative controls within the rejecting tissue.
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58 |
23798565
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Suppression is associated with development of a regulatory population of donor CD4(+) CD25(+)T-cells that express high levels of cytotoxic T-lymphocyte antigen 4 (CTLA-4).
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59 |
23798565
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Suppression is associated with development of a regulatory population of donor CD4(+) CD25(+)T-cells that express high levels of cytotoxic T-lymphocyte antigen 4 (CTLA-4).
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60 |
23798565
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CTLA-4 is a negative regulator of T-cell responses and is associated with the induction of tolerogenic dendritic cells (DCs) that produce indoleamine 2,3-dioxygenase (IDO).
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61 |
23798565
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CTLA-4 is a negative regulator of T-cell responses and is associated with the induction of tolerogenic dendritic cells (DCs) that produce indoleamine 2,3-dioxygenase (IDO).
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62 |
23798565
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Here, we show that despite increased expression of Ifng, Irf3, Irf7, Ido1, and Ido2 in the lymph nodes of TCDD-treated host mice, inhibition of IDO enzyme activity by 1-methyl-tryptophan was unable to relieve TCDD-mediated suppression of the GVH response.
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63 |
23798565
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Here, we show that despite increased expression of Ifng, Irf3, Irf7, Ido1, and Ido2 in the lymph nodes of TCDD-treated host mice, inhibition of IDO enzyme activity by 1-methyl-tryptophan was unable to relieve TCDD-mediated suppression of the GVH response.
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64 |
22295566
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Complex association analysis of copaxone (glatiramer acetate) immunotherapy efficacy with allelic polymorphism in the number of immune response genes, which encode interferone beta (IFNB1), transforming growth factor beta1 (TGFB1), interferone gamma (IFNG), tumor necrosis factor (TNF), interferon alpha/beta receptor 1 (IFNAR1), CC chemokine receptor 5 (CCR5), interleukin 7 receptor alpha subunit (IL7RA), cytotoxic T-lymphocyte antigen 4 (CTLA4) and HLA class II histocompatibility antigen beta chain (DRB1) was performed with APSampler algorithm for 285 multiple sclerosis patients of Russian ethnicity.
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65 |
22295566
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Complex association analysis of copaxone (glatiramer acetate) immunotherapy efficacy with allelic polymorphism in the number of immune response genes, which encode interferone beta (IFNB1), transforming growth factor beta1 (TGFB1), interferone gamma (IFNG), tumor necrosis factor (TNF), interferon alpha/beta receptor 1 (IFNAR1), CC chemokine receptor 5 (CCR5), interleukin 7 receptor alpha subunit (IL7RA), cytotoxic T-lymphocyte antigen 4 (CTLA4) and HLA class II histocompatibility antigen beta chain (DRB1) was performed with APSampler algorithm for 285 multiple sclerosis patients of Russian ethnicity.
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66 |
22295566
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The results show evidence for the contribution of polymorphic variants in CCRS, DRB1, IFNG, TGFB1, IFNAR1, IL7RA and, probably, TNF and CTLA4 genes to copaxone treatment response.
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67 |
22295566
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The results show evidence for the contribution of polymorphic variants in CCRS, DRB1, IFNG, TGFB1, IFNAR1, IL7RA and, probably, TNF and CTLA4 genes to copaxone treatment response.
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68 |
22295566
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Single alleles of CCR5 and DRB1 genes are reliably associated with treatment efficacy.
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69 |
22295566
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Single alleles of CCR5 and DRB1 genes are reliably associated with treatment efficacy.
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70 |
20018909
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Blood and decidual CD4(+) T cells from 18 healthy first-trimester pregnant women were analyzed for expression of Treg-cell markers (CD25, FOXP3, CD127, CTLA4, and human leukocyte antigen-DR [HLA-DR]), chemokine receptors (CCR4, CCR6, and CXCR3), and the proliferation antigen MKI67 by six-color flow cytometry.
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71 |
20018909
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Using chemokine receptor expression profiles of CCR4, CCR6, and CXCR3 as markers for T(H)1, T(H)2, and T(H)17 cells, we showed that T(H)17 cells were nearly absent in decidua, whereas T(H)2-cell frequencies were similar in blood and decidua.
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72 |
20018909
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CCR6(+) T(H)1 cells, reported to secrete high levels of interferon gamma (IFNG), were fewer, whereas the moderately IFNG-secreting CCR6(-) T(H)1 cells were more frequent in decidua compared with blood.
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73 |
19494038
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Here, we present a comprehensive analysis of differential DNA methylation in human conventional CD4(+) T cells (Tconv) and CD4(+)CD25(+) regulatory T cells (Treg), cell types whose differentiation and function are known to be controlled by epigenetic mechanisms.
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74 |
19494038
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More than 100 differentially methylated regions (DMRs) were identified that are present mainly in cell type-specific genes (e.g., FOXP3, IL2RA, CTLA4, CD40LG, and IFNG) and show differential patterns of histone H3 lysine 4 methylation.
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75 |
18337305
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New approach reveals CD28 and IFNG gene interaction in the susceptibility to cervical cancer.
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76 |
18337305
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A total of 14 single nucleotide polymorphisms (SNPs) distributed in CD28, CTLA4, ICOS, PDCD1, FAS, TNFA, IL6, IFNG, TGFB1 and IL10 genes were determined in patients and healthy individuals from three independent case/control sets.
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77 |
18337305
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The multi-locus analysis revealed higher frequencies in cancer patients of three three-genotype combinations [CD28+17(TT)/IFNG+874(AA)/TNFA-308(GG), CD28+17(TT)/IFN+847(AA)/PDCD1+7785(CT), and CD28 +17(TT)/IFNG+874(AA)/ICOS+1564(TT)] (P < 0.01, Monte Carlo simulation).
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78 |
18337305
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We hypothesized that this two-genotype [CD28(TT) and IFNG(AA)] combination could have a major contribution to the observed association.
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79 |
18337305
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To address this question, we analyzed the frequency of the CD28(TT), IFNG(AA) genotype combination in the three groups combined, and observed its increase in patients (P = 0.0011 by Fisher's exact test).
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80 |
18337305
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Further analysis suggested that gene-gene interaction between CD28 and IFNG might contribute to susceptibility to cervical cancer.
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81 |
18337305
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Our results showed an epistatic effect between CD28 and IFNG genes in susceptibility to cervical cancer, a finding that might be relevant for a better understanding of the disease pathogenesis.
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