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  1. Article ; Online: Defining the Molecular Hallmarks of T-Cell Memory.

    Zebley, Caitlin C / Akondy, Rama S / Youngblood, Benjamin A / Kissick, Haydn T

    Cold Spring Harbor perspectives in biology

    2022  Volume 14, Issue 3

    Abstract: The pool of memory CD8 T cells is comprised of highly specialized subpopulations of cells with both shared and distinct functions. The ongoing study of T-cell memory is focused on how these different subpopulations arise, how the cells are maintained ... ...

    Abstract The pool of memory CD8 T cells is comprised of highly specialized subpopulations of cells with both shared and distinct functions. The ongoing study of T-cell memory is focused on how these different subpopulations arise, how the cells are maintained over the life of the host, and how the cells protect a host against reinfection. As a field we have used the convenience of a narrow range of surface markers to define and study these memory T-cell subsets. However, as we learn more about these cells, it is becoming clear that these broad definitions are insufficient to capture the complexity of the CD8 memory T-cell pool, and an updated definition of these cellular states are needed. Here, we discuss data that have recently arisen that highlight the difficulty in using surface markers to functionally characterize CD8 T-cell populations, and the possibility of using the epigenetic state of cells to more clearly define the functional capacity of CD8 memory T-cell subsets.
    MeSH term(s) CD8-Positive T-Lymphocytes/physiology ; Immunologic Memory ; Memory T Cells ; T-Lymphocyte Subsets
    Language English
    Publishing date 2022-03-01
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 1943-0264
    ISSN (online) 1943-0264
    DOI 10.1101/cshperspect.a037804
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Stem, Effector, and Hybrid States of Memory CD8

    Lugli, Enrico / Galletti, Giovanni / Boi, Shannon K / Youngblood, Benjamin A

    Trends in immunology

    2019  Volume 41, Issue 1, Page(s) 17–28

    Abstract: ... ...

    Abstract CD8
    MeSH term(s) Antigens/immunology ; CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/immunology ; Cell Differentiation ; Epigenesis, Genetic/immunology ; Humans ; Immunologic Memory/genetics ; Immunologic Memory/immunology
    Chemical Substances Antigens
    Language English
    Publishing date 2019-12-04
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2036831-8
    ISSN 1471-4981 ; 1471-4906
    ISSN (online) 1471-4981
    ISSN 1471-4906
    DOI 10.1016/j.it.2019.11.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Functional T cells are capable of supernumerary cell division and longevity.

    Soerens, Andrew G / Künzli, Marco / Quarnstrom, Clare F / Scott, Milcah C / Swanson, Lee / Locquiao, J J / Ghoneim, Hazem E / Zehn, Dietmar / Youngblood, Benjamin / Vezys, Vaiva / Masopust, David

    Nature

    2023  Volume 614, Issue 7949, Page(s) 762–766

    Abstract: Differentiated somatic mammalian cells putatively exhibit species-specific division limits that impede cancer but may constrain ... ...

    Abstract Differentiated somatic mammalian cells putatively exhibit species-specific division limits that impede cancer but may constrain lifespans
    MeSH term(s) Animals ; Mice ; CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/immunology ; Cell Differentiation ; Cell Division ; Immunologic Memory ; Longevity/immunology ; Neoplasms/immunology ; Neoplasms/pathology ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology ; Cellular Senescence/immunology ; Cellular Senescence/physiology ; Lymphocyte Activation ; Immunization, Secondary ; Vaccination ; Adoptive Transfer ; Time Factors ; Infections/immunology ; Chronic Disease ; Epigenesis, Genetic
    Chemical Substances Pdcd1 protein, mouse
    Language English
    Publishing date 2023-01-18
    Publishing country England
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-022-05626-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Phase I Clinical Trial of DNA Methyltransferase Inhibitor Decitabine and PARP Inhibitor Talazoparib Combination Therapy in Relapsed/Refractory Acute Myeloid Leukemia.

    Baer, Maria R / Kogan, Aksinija A / Bentzen, Søren M / Mi, Tian / Lapidus, Rena G / Duong, Vu H / Emadi, Ashkan / Niyongere, Sandrine / O'Connell, Casey L / Youngblood, Benjamin A / Baylin, Stephen B / Rassool, Feyruz V

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2022  Volume 28, Issue 7, Page(s) 1313–1322

    Abstract: Purpose: Patients with acute myeloid leukemia (AML) unfit for, or resistant to, intensive chemotherapy are often treated with DNA methyltransferase inhibitors (DNMTi). Novel combinations may increase efficacy. In addition to demethylating CpG island ... ...

    Abstract Purpose: Patients with acute myeloid leukemia (AML) unfit for, or resistant to, intensive chemotherapy are often treated with DNA methyltransferase inhibitors (DNMTi). Novel combinations may increase efficacy. In addition to demethylating CpG island gene promoter regions, DNMTis enhance PARP1 recruitment and tight binding to chromatin, preventing PARP-mediated DNA repair, downregulating homologous recombination (HR) DNA repair, and sensitizing cells to PARP inhibitor (PARPi). We previously demonstrated DNMTi and PARPi combination efficacy in AML in vitro and in vivo. Here, we report a phase I clinical trial combining the DNMTi decitabine and the PARPi talazoparib in relapsed/refractory AML.
    Patients and methods: Decitabine and talazoparib doses were escalated using a 3 + 3 design. Pharmacodynamic studies were performed on cycle 1 days 1 (pretreatment), 5 and 8 blood blasts.
    Results: Doses were escalated in seven cohorts [25 patients, including 22 previously treated with DNMTi(s)] to a recommended phase II dose combination of decitabine 20 mg/m2 intravenously daily for 5 or 10 days and talazoparib 1 mg orally daily for 28 days, in 28-day cycles. Grade 3-5 events included fever in 19 patients and lung infections in 15, attributed to AML. Responses included complete remission with incomplete count recovery in two patients (8%) and hematologic improvement in three. Pharmacodynamic studies showed the expected DNA demethylation, increased PARP trapping in chromatin, increased γH2AX foci, and decreased HR activity in responders. γH2AX foci increased significantly with increasing talazoparib doses combined with 20 mg/m2 decitabine.
    Conclusions: Decitabine/talazoparib combination was well tolerated. Expected pharmacodynamic effects occurred, especially in responders.
    MeSH term(s) Antineoplastic Combined Chemotherapy Protocols ; Azacitidine ; DNA ; Decitabine/therapeutic use ; Humans ; Leukemia, Myeloid, Acute/drug therapy ; Methyltransferases ; Phthalazines ; Poly(ADP-ribose) Polymerase Inhibitors/therapeutic use
    Chemical Substances Phthalazines ; Poly(ADP-ribose) Polymerase Inhibitors ; Decitabine (776B62CQ27) ; DNA (9007-49-2) ; talazoparib (9QHX048FRV) ; Methyltransferases (EC 2.1.1.-) ; Azacitidine (M801H13NRU)
    Language English
    Publishing date 2022-01-28
    Publishing country United States
    Document type Clinical Trial, Phase I ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-21-3729
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Safety, Outcomes, and T-Cell Characteristics in Patients with Relapsed or Refractory MDS or CMML Treated with Atezolizumab in Combination with Guadecitabine.

    O'Connell, Casey L / Baer, Maria R / Ørskov, Andreas Due / Saini, Sunil Kumar / Duong, Vu H / Kropf, Patricia / Hansen, Jakob Werner / Tsao-Wei, Denice / Jang, Hyo Sik / Emadi, Ashkan / Holmberg-Thyden, Staffan / Cowland, Jack / Brinker, Brett T / Horwood, Kristin / Burgos, Ryan / Hostetter, Galen / Youngblood, Benjamin A / Hadrup, Sine Reker / Issa, Jean-Pierre /
    Jones, Peter / Baylin, Stephen B / Siddiqi, Imran / Grønbaek, Kirsten

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2022  Volume 28, Issue 24, Page(s) 5306–5316

    Abstract: Purpose: We hypothesized that resistance to hypomethylating agents (HMA) among patients with myelodysplastic syndrome (MDS) and chronic myelomonocytic leukemia (CMML) would be overcome by combining a programmed death-ligand 1 antibody with an HMA.: ... ...

    Abstract Purpose: We hypothesized that resistance to hypomethylating agents (HMA) among patients with myelodysplastic syndrome (MDS) and chronic myelomonocytic leukemia (CMML) would be overcome by combining a programmed death-ligand 1 antibody with an HMA.
    Patients and methods: We conducted a Phase I/II, multicenter clinical trial for patients with MDS not achieving an International Working Group response after at least 4 cycles of an HMA ("refractory") or progressing after a response ("relapsed") with 3+ or higher risk MDS by the revised International Prognostic Scoring System (IPSS-R) and CMML-1 or -2. Phase I consisted of a 3+3 dose-escalation design beginning with guadecitabine at 30 mg/m2 and escalating to 60 mg/m2 Days 1 to 5 with fixed-dose atezolizumab: 840 mg intravenously Days 8 and 22 of a 28-day cycle. Primary endpoints were safety and tolerability; secondary endpoints were overall response rate (ORR) and survival.
    Results: Thirty-three patients, median age 73 (range 54-85), were treated. Thirty patients had MDS and 3 had CMML, with 30% relapsed and 70% refractory. No dose-limiting toxicities were observed in Phase I. There were 3 (9%) deaths in ≤ 30 days. Five patients (16%) came off study for drug-related toxicity. Immune-related adverse events (IRAE) occurred in 12 (36%) patients (4 grade 3, 3 grade 2, and 5 grade1). ORR was 33% [95% confidence interval (CI), 19%-52%] with 2 complete remission (CR), 3 hematologic improvement, 5 marrow CR, and 1 partial remission. Median overall survival was 15.1 (95% CI, 8.5-25.3) months.
    Conclusions: Guadecitabine with atezolizumab has modest efficacy with manageable IRAEs and typical cytopenia-related safety concerns for patients with relapsed or refractory MDS and CMML.
    MeSH term(s) Humans ; Aged ; Leukemia, Myelomonocytic, Chronic/drug therapy ; Treatment Outcome ; T-Lymphocytes ; Myelodysplastic Syndromes/drug therapy
    Chemical Substances guadecitabine (2KT4YN1DP7) ; atezolizumab (52CMI0WC3Y)
    Language English
    Publishing date 2022-11-11
    Publishing country United States
    Document type Clinical Trial, Phase I ; Multicenter Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-22-1810
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Developmental plasticity allows outside-in immune responses by resident memory T cells.

    Fonseca, Raissa / Beura, Lalit K / Quarnstrom, Clare F / Ghoneim, Hazem E / Fan, Yiping / Zebley, Caitlin C / Scott, Milcah C / Fares-Frederickson, Nancy J / Wijeyesinghe, Sathi / Thompson, Emily A / Borges da Silva, Henrique / Vezys, Vaiva / Youngblood, Benjamin / Masopust, David

    Nature immunology

    2020  Volume 21, Issue 4, Page(s) 412–421

    Abstract: Central memory T ( ... ...

    Abstract Central memory T (T
    MeSH term(s) Animals ; Cell Differentiation/immunology ; Cell Plasticity/immunology ; Female ; Immunologic Memory/immunology ; Intestinal Mucosa/immunology ; Intestine, Small/immunology ; Mice ; Mice, Inbred C57BL ; T-Lymphocyte Subsets/immunology
    Keywords covid19
    Language English
    Publishing date 2020-02-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-020-0607-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Global DNA methylation remodeling accompanies CD8 T cell effector function.

    Scharer, Christopher D / Barwick, Benjamin G / Youngblood, Benjamin A / Ahmed, Rafi / Boss, Jeremy M

    Journal of immunology (Baltimore, Md. : 1950)

    2013  Volume 191, Issue 6, Page(s) 3419–3429

    Abstract: The differentiation of CD8 T cells in response to acute infection results in the acquisition of hallmark phenotypic effector functions; however, the epigenetic mechanisms that program this differentiation process on a genome-wide scale are largely ... ...

    Abstract The differentiation of CD8 T cells in response to acute infection results in the acquisition of hallmark phenotypic effector functions; however, the epigenetic mechanisms that program this differentiation process on a genome-wide scale are largely unknown. In this article, we report the DNA methylomes of Ag-specific naive and day-8 effector CD8 T cells following acute lymphocytic choriomeningitis virus infection. During effector CD8 T cell differentiation, DNA methylation was remodeled such that changes in DNA methylation at gene promoter regions correlated negatively with gene expression. Importantly, differentially methylated regions were enriched at cis-elements, including enhancers active in naive T cells. Differentially methylated regions were associated with cell type-specific transcription factor binding sites, and these transcription factors clustered into modules that define networks targeted by epigenetic regulation and control of effector CD8 T cell function. Changes in the DNA methylation profile following CD8 T cell activation revealed numerous cellular processes, cis-elements, and transcription factor networks targeted by DNA methylation. Together, the results demonstrated that DNA methylation remodeling accompanies the acquisition of the CD8 T cell effector phenotype and repression of the naive cell state. Therefore, these data provide the framework for an epigenetic mechanism that is required for effector CD8 T cell differentiation and adaptive immune responses.
    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/immunology ; Cell Differentiation/genetics ; Cell Differentiation/immunology ; DNA Methylation/genetics ; DNA Methylation/immunology ; Epigenesis, Genetic/genetics ; Epigenesis, Genetic/immunology ; Immunoprecipitation ; Lymphocyte Activation/genetics ; Lymphocyte Activation/immunology ; Mice ; Mice, Transgenic ; Molecular Sequence Data
    Language English
    Publishing date 2013-08-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.1301395
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Preferential expansion of CD8+ CD19-CAR T cells postinfusion and the role of disease burden on outcome in pediatric B-ALL.

    Talleur, Aimee C / Qudeimat, Amr / Métais, Jean-Yves / Langfitt, Deanna / Mamcarz, Ewelina / Crawford, Jeremy Chase / Huang, Sujuan / Cheng, Cheng / Hurley, Caitlin / Madden, Renee / Sharma, Akshay / Suliman, Ali / Srinivasan, Ashok / Velasquez, M Paulina / Obeng, Esther A / Willis, Catherine / Akel, Salem / Karol, Seth E / Inaba, Hiroto /
    Bragg, Allison / Zheng, Wenting / Zhou, Sheng M / Schell, Sarah / Tuggle-Brown, MaCal / Cullins, David / Patil, Sagar L / Li, Ying / Thomas, Paul G / Zebley, Caitlin / Youngblood, Benjamin / Pui, Ching-Hon / Lockey, Timothy / Geiger, Terrence L / Meagher, Michael M / Triplett, Brandon M / Gottschalk, Stephen

    Blood advances

    2022  Volume 6, Issue 21, Page(s) 5737–5749

    Abstract: T cells expressing CD19-specific chimeric antigen receptors (CD19-CARs) have potent antileukemia activity in pediatric and adult patients with relapsed and/or refractory B-cell acute lymphoblastic leukemia (B-ALL). However, not all patients achieve a ... ...

    Abstract T cells expressing CD19-specific chimeric antigen receptors (CD19-CARs) have potent antileukemia activity in pediatric and adult patients with relapsed and/or refractory B-cell acute lymphoblastic leukemia (B-ALL). However, not all patients achieve a complete response (CR), and a significant percentage relapse after CD19-CAR T-cell therapy due to T-cell intrinsic and/or extrinsic mechanisms. Thus, there is a need to evaluate new CD19-CAR T-cell products in patients to improve efficacy. We developed a phase 1/2 clinical study to evaluate an institutional autologous CD19-CAR T-cell product in pediatric patients with relapsed/refractory B-ALL. Here we report the outcome of the phase 1 study participants (n = 12). Treatment was well tolerated, with a low incidence of both cytokine release syndrome (any grade, n = 6) and neurotoxicity (any grade, n = 3). Nine out of 12 patients (75%) achieved a minimal residual disease-negative CR in the bone marrow (BM). High disease burden (≥40% morphologic blasts) before CAR T-cell infusion correlated with increased side effects and lower response rate, but not with CD19-CAR T-cell expansion. After infusion, CD8+ CAR T cells had a proliferative advantage over CD4+ CAR T cells and at peak expansion, had an effector memory phenotype with evidence of antigen-driven differentiation. Patients that proceeded to allogeneic hematopoietic cell transplantation (AlloHCT) had sustained, durable responses. In summary, the initial evaluation of our institutional CD19-CAR T-cell product demonstrates safety and efficacy while highlighting the impact of pre-infusion disease burden on outcomes. This trial was registered at www.clinicaltrials.gov as #NCT03573700.
    MeSH term(s) Humans ; Antigens, CD19 ; Burkitt Lymphoma ; CD8-Positive T-Lymphocytes ; Cost of Illness ; Lymphoma, B-Cell ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/therapy ; Receptors, Chimeric Antigen ; T-Lymphocytes
    Chemical Substances Antigens, CD19 ; Receptors, Chimeric Antigen
    Language English
    Publishing date 2022-04-21
    Publishing country United States
    Document type Clinical Trial, Phase I ; Clinical Trial, Phase II ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2915908-8
    ISSN 2473-9537 ; 2473-9529
    ISSN (online) 2473-9537
    ISSN 2473-9529
    DOI 10.1182/bloodadvances.2021006293
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Defining 'T cell exhaustion'.

    Blank, Christian U / Haining, W Nicholas / Held, Werner / Hogan, Patrick G / Kallies, Axel / Lugli, Enrico / Lynn, Rachel C / Philip, Mary / Rao, Anjana / Restifo, Nicholas P / Schietinger, Andrea / Schumacher, Ton N / Schwartzberg, Pamela L / Sharpe, Arlene H / Speiser, Daniel E / Wherry, E John / Youngblood, Benjamin A / Zehn, Dietmar

    Nature reviews. Immunology

    2019  Volume 19, Issue 11, Page(s) 665–674

    Abstract: T cell exhaustion' is a broad term that has been used to describe the response of T cells to chronic antigen stimulation, first in the setting of chronic viral infection but more recently in response to tumours. Understanding the features of and ... ...

    Abstract 'T cell exhaustion' is a broad term that has been used to describe the response of T cells to chronic antigen stimulation, first in the setting of chronic viral infection but more recently in response to tumours. Understanding the features of and pathways to exhaustion has crucial implications for the success of checkpoint blockade and adoptive T cell transfer therapies. In this Viewpoint article, 18 experts in the field tell us what exhaustion means to them, ranging from complete lack of effector function to altered functionality to prevent immunopathology, with potential differences between cancer and chronic infection. Their responses highlight the dichotomy between terminally differentiated exhausted T cells that are TCF1
    MeSH term(s) Animals ; Hepatocyte Nuclear Factor 1-alpha/physiology ; High Mobility Group Proteins/physiology ; Humans ; Infections/immunology ; Neoplasms/immunology ; Programmed Cell Death 1 Receptor/physiology ; T-Lymphocytes/immunology
    Chemical Substances HNF1A protein, human ; Hepatocyte Nuclear Factor 1-alpha ; High Mobility Group Proteins ; Programmed Cell Death 1 Receptor ; TOX protein, human
    Language English
    Publishing date 2019-09-30
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/s41577-019-0221-9
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  10. Article ; Online: Blimp-1 represses CD8 T cell expression of PD-1 using a feed-forward transcriptional circuit during acute viral infection.

    Lu, Peiyuan / Youngblood, Benjamin A / Austin, James W / Mohammed, Ata Ur Rasheed / Butler, Royce / Ahmed, Rafi / Boss, Jeremy M

    The Journal of experimental medicine

    2014  Volume 211, Issue 3, Page(s) 515–527

    Abstract: Programmed cell death 1 (PD-1) is an inhibitory immune receptor that regulates T cell function, yet the molecular events that control its expression are largely unknown. We show here that B lymphocyte-induced maturation protein 1 (Blimp-1)-deficient CD8 ... ...

    Abstract Programmed cell death 1 (PD-1) is an inhibitory immune receptor that regulates T cell function, yet the molecular events that control its expression are largely unknown. We show here that B lymphocyte-induced maturation protein 1 (Blimp-1)-deficient CD8 T cells fail to repress PD-1 during the early stages of CD8 T cell differentiation after acute infection with lymphocytic choriomeningitis virus (LCMV) strain Armstrong. Blimp-1 represses PD-1 through a feed-forward repressive circuit by regulating PD-1 directly and by repressing NFATc1 expression, an activator of PD-1 expression. Blimp-1 binding induces a repressive chromatin structure at the PD-1 locus, leading to the eviction of NFATc1 from its site. These data place Blimp-1 at an important phase of the CD8 T cell effector response and provide a molecular mechanism for its repression of PD-1.
    MeSH term(s) Animals ; Arenaviridae Infections/immunology ; Binding Sites/genetics ; CD8-Positive T-Lymphocytes/metabolism ; Cell Line, Tumor ; Chromatin Immunoprecipitation ; DNA Primers/genetics ; Gene Expression Regulation/immunology ; Luciferases ; Lymphocytic choriomeningitis virus/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NFATC Transcription Factors/metabolism ; Positive Regulatory Domain I-Binding Factor 1 ; Programmed Cell Death 1 Receptor/metabolism ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Transcription Factors/deficiency ; Transcription Factors/genetics ; Transcription Factors/immunology
    Chemical Substances DNA Primers ; NFATC Transcription Factors ; Nfatc1 protein, mouse ; Pdcd1 protein, mouse ; Prdm1 protein, mouse ; Programmed Cell Death 1 Receptor ; Transcription Factors ; Luciferases (EC 1.13.12.-) ; Positive Regulatory Domain I-Binding Factor 1 (EC 2.1.1.-)
    Language English
    Publishing date 2014-03-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20130208
    Database MEDical Literature Analysis and Retrieval System OnLINE

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