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  • 1
    Online Resource
    Online Resource
    Type 17 immunity promotes the exhaustion of CD8 + T cells in cancer
    BMJ ; 2021
    In:  Journal for ImmunoTherapy of Cancer Vol. 9, No. 6 ( 2021-06), p. e002603-
    Details
    In: Journal for ImmunoTherapy of Cancer, BMJ, Vol. 9, No. 6 ( 2021-06), p. e002603-
    Abstract: Multiple types of immune cells producing IL-17 are found in the tumor microenvironment. However, their roles in tumor progression and exhaustion of CD8 + tumor-infiltrating lymphocytes (TILs) remain unclear. Methods To determine the role of type 17 immunity in tumor, we investigated the growth of B16F10 melanoma and the exhaustion of CD8 + TILs in Il17a −/− mice, Il17a Cre R26 DTA mice, RORγt inhibitor-treated mice, or their respective control mice. Adoptive transfer of tumor-specific IL-17-producing T cells was performed in B16F10-bearing congenic mice. Anti-CD4 or anti-Ly6G antibodies were used to deplete CD4 + T cells or CD11b + Gr-1 hi myeloid cells in vivo , respectively. Correlation between type 17 immunity and T cell exhaustion in human cancer was evaluated by interrogating TCGA dataset. Results Depletion of CD4 + T cells promotes the exhaustion of CD8 + T cells with a concomitant increase in IL-17-producing CD8 + T (Tc17) cells in the tumor. Unlike IFN-γ-producing CD8 + T (Tc1) cells, tumor-infiltrating Tc17 cells exhibit CD103 + KLRG1 − IL-7Rα hi tissue resident memory-like phenotypes and are poorly cytolytic. Adoptive transfer of IL-17-producing tumor-specific T cells increases, while depletion of IL-17-producing cells decreases, the frequency of PD-1 hi Tim3 + TOX + terminally exhausted CD8 + T cells in the tumor. Blockade of IL-17 or RORγt pathway inhibits exhaustion of CD8 + T cells and also delays tumor growth in vivo . Consistent with these results, human TCGA analyses reveal a strong positive correlation between type 17 and CD8 + T cell exhaustion signature gene sets in multiple cancers. Conclusion IL-17-producing cells promote terminal exhaustion of CD8 + T cells and tumor progression in vivo , which can be reversed by blockade of IL-17 or RORγt pathway. These findings unveil a novel role for IL-17-producing cells as tumor-promoting cells facilitating CD8 + T cell exhaustion, and propose type 17 immunity as a promising target for cancer immunotherapy.
    Type of Medium: Online Resource
    ISSN: 2051-1426
    URL: Article
    DOI: 10.1136/jitc-2021-002603
    Language: English
    Publisher: BMJ
    Publication Date: 2021
    detail.hit.zdb_id: 2719863-7
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  • 2
    Online Resource
    Online Resource
    Myeloid derived suppressor cells(MDSCs) emergence from distinct splenic precursors (162.28)
    The American Association of Immunologists ; 2012
    In:  The Journal of Immunology Vol. 188, No. 1_Supplement ( 2012-05-01), p. 162.28-162.28
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 188, No. 1_Supplement ( 2012-05-01), p. 162.28-162.28
    Abstract: Myeloid derived suppressor cells(MDSCs) are a heterogenous population of immature myeloid cells, which accumulate in various pathological conditions, especially in tumor. In mice, MDSCs are characterized by the co-expression of Gr1 and CD11b molecules, and these cells could be classified into two subsets, CD11b+Ly6G+Ly6Clow polymorphonuclear neutrophil-like(PMN) MDSCs and CD11b+Ly6G-Ly6Chigh monocytic(Mo) MDSCs, by their expression of Ly6C and Ly6G molecules. Functional characteristics and fate of MDSCs are defined quite well. On the other hands, accumulation mechanism and origins of MDSC need to be more elucidated, and have not been fully understood whether MDSC could be generated in the periphery from distinct precursors in tumor microenvironment. For the first time, we identified the presence of splenic MDSC precursors in tumor bearing mice, characterized by CD11b+Ly6G-Ly6Cneg/low. We demonstrated that cytokines related to MDSC accumulation convert CD11b+Ly6G-Ly6Cneg/low cells into CD11b+Ly6G+Ly6Clow PMN-MDSC and/or CD11b+Ly6G-Ly6Chigh Mo-MDSC. These converted cells exerted strong suppressive activity on DO11.10 Tg splenocytes proliferation. Thus, these data suggest that there are peripheral distinct precursors, CD11b+Ly6Cneg/low cells, from which immunosuppressive MDSC could be generated.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.188.Supp.162.28
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2012
    detail.hit.zdb_id: 1475085-5
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  • 3
    Online Resource
    Online Resource
    Tumor Microenvironmental Conversion of Natural Killer Cells into Myeloid-Derived Suppressor Cells
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 18 ( 2013-09-15), p. 5669-5681
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 18 ( 2013-09-15), p. 5669-5681
    Abstract: How myeloid-derived suppressor cells (MDSC) emerge in the tumor environment remains unclear. Here, we report that GM-CSF can convert natural killer (NK) cells into MDSCs. When transferred into tumor-bearing mice, adoptively transferred NK cells lost their NK phenotype and were converted into Ly6ChighLy6Ghigh MDSC. This conversion was abolished by exposure to IL-2 either in vitro or in vivo. Notably, we found that of the 4 maturation stages based on CD11b/CD27 expression levels, only the CD11bhighCD27high NK cells could be converted into CD11b+Gr1+ MDSC ex vivo. Transfer of CD27high NK cells from tumor-bearing mice into tumor-bearing recipients was associated with conversion to MDSC in a manner associated with reduced numbers of CD11bhighCD27high and CD11bhighCD27low NK cell populations in the recipients. Our results identify a pathway of MDSC development from immature NK cells in tumor-bearing hosts, providing new insights into how tumor cells modulate their host immune microenvironment to escape immune surveillance. Cancer Res; 73(18); 5669–81. ©2013 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-13-0545
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 4
    Online Resource
    Online Resource
    Conversion of Th2 memory cells into Foxp3 + regulatory T cells suppressing Th2-mediated allergic asthma
    Proceedings of the National Academy of Sciences ; 2010
    In:  Proceedings of the National Academy of Sciences Vol. 107, No. 19 ( 2010-05-11), p. 8742-8747
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 107, No. 19 ( 2010-05-11), p. 8742-8747
    Abstract: Genetic and epigenetic programming of T helper (Th) cell subsets during their polarization from naive Th cells establishes long-lived memory Th cells that stably maintain their lineage signatures. However, whether memory Th cells can be redifferentiated into another Th lineage is unclear. In this study, we show that Ag-specific memory Th cells were redifferentiated into Foxp3 + T cells by TGF-β when stimulated in the presence of all-trans retinoic acid and rapamycin. The “converted” Foxp3 + T cells that were derived from Th2 memory cells down-regulated GATA-3 and IRF4 and produced little IL-4, IL-5, and IL-13. Instead, the converted Foxp3 + T cells suppressed the proliferation and cytokine production of Th2 memory cells. More importantly, the converted Foxp3 + T cells efficiently accumulated in the airways and significantly suppressed Th2 memory cell-mediated airway hyperreactivity, eosinophilia, and allergen-specific IgE production. Our findings reveal the plasticity of Th2 memory cells and provide a strategy for adoptive immunotherapy for the treatment of allergic diseases.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0911756107
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2010
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 5
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    Online Resource
    Phenotypical and functional changes in myeloid-derived suppressor cells during the tumor progression: FKBP51 regulates the suppressive function of MDSCs (66.25)
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 186, No. 1_Supplement ( 2011-04-01), p. 66.25-66.25
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 186, No. 1_Supplement ( 2011-04-01), p. 66.25-66.25
    Abstract: Immature myeloid cells which are increased by tumor-derived factors actively suppress immune cells. Therefore, they are called as myeloid-derived suppressor cells (MDSCs). Since the effect of cancer immunotherapy would be enhanced by removing MDSCs or inhibiting their suppressive function, we tried to find a target for MDSC regulation. MDSCs were increased during the tumor progression and MDSCs of late stage tumor bearing mice had stronger suppressive activity than those of early stage tumor bearing mice, in T cell proliferation assays. To find factors that change the MDSCs during the tumor progression, we analyzed gene expression profiles in MDSCs at various tumor stages and found that expression of Fkbp5 was increased in the Mo- and PMN- MDSCs of late stage tumor bearing mice. By means of rapamycin, which inhibit the PPIase function of FKBP51 protein, we demonstrate that the FKBP51 was involved in the suppressive function of MDSCs via regulation of iNOS expression. In addition, the FKBP51 enhanced the survival of MDSCs. By targeting the FKBP51, we may regulate the suppressive function of MDSCs and enhance the effect of anti-cancer immunotherapy.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.186.Supp.66.25
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2011
    detail.hit.zdb_id: 1475085-5
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  • 6
    Online Resource
    Online Resource
    Fibrinogen cleavage products and Toll-like receptor 4 promote the generation of programmed cell death 1 ligand 2–positive dendritic cells in allergic asthma
    Elsevier BV ; 2018
    In:  Journal of Allergy and Clinical Immunology Vol. 142, No. 2 ( 2018-08), p. 530-541.e6
    Details
    In: Journal of Allergy and Clinical Immunology, Elsevier BV, Vol. 142, No. 2 ( 2018-08), p. 530-541.e6
    Type of Medium: Online Resource
    ISSN: 0091-6749
    URL: Article
    DOI: 10.1016/j.jaci.2017.09.019
    RVK:
    XA 52000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2018
    detail.hit.zdb_id: 2006613-2
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  • 7
    Online Resource
    Online Resource
    Functional Changes in Myeloid-Derived Suppressor Cells (MDSCs) during Tumor Growth: FKBP51 Contributes to the Regulation of the Immunosuppressive Function of MDSCs
    The American Association of Immunologists ; 2012
    In:  The Journal of Immunology Vol. 188, No. 9 ( 2012-05-01), p. 4226-4234
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 188, No. 9 ( 2012-05-01), p. 4226-4234
    Abstract: Myeloid-derived suppressor cells (MDSCs) are increased by tumor-derived factors and suppress anti-tumor immunity. MDSCs obtained at a late time point after tumor injection had stronger suppressive activity than MDSCs obtained at an early time point, as measured by T cell proliferation assays. To find factors in MDSCs that change during tumor growth, we analyzed gene expression profiles from MDSCs at different time points after tumor injection. We found that immune response-related genes were downregulated but protumor function-related genes were upregulated in both monocytic MDSCs (Mo-MDSCs) and polymorphonuclear granulocytic MDSCs (PMN-MDSCs) at the late time point. Among differentially expressed genes, FK506 binding protein 51 (FKBP51), which is a member of the immunophilin protein family and plays a role in immunoregulation, was increased in the Mo-MDSCs and PMN-MDSCs isolated from the late time points. Experiments using small interfering RNA and a chemical inhibitor of FKBP51 revealed that FKBP51 contributes to the regulation of the suppressive function of MDSCs by increasing inducible NO synthase, arginase-1, and reactive oxygen species levels and enhancing NF-κB activity. Collectively, our data suggest that FKBP51 is a novel molecule that can be targeted to regulate the immunosuppressive function of MDSCs.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1103040
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2012
    detail.hit.zdb_id: 1475085-5
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  • 8
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    Online Resource
    Oltipraz inhibits TGF-{beta}-mediated Foxp3+ regulatory T cell differentiation (139.15)
    The American Association of Immunologists ; 2010
    In:  The Journal of Immunology Vol. 184, No. 1_Supplement ( 2010-04-01), p. 139.15-139.15
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 184, No. 1_Supplement ( 2010-04-01), p. 139.15-139.15
    Abstract: Oltipraz [5-(2-pyrazinyl)-4-methyl-1,2-dithiol-3-thione] is a synthetic dithiolethione that has been widely studied for the prevention of cancer formation as well as treatment of liver cirrhosis. Although the precise mechanism by which oltipraz inhibits cancer and liver diseases remains unknown, it may be attributed to its ability to induce the expression of numerous Phase 2 detoxification enzymes and to reduce hepatic triglyceride accumulation by S6K1-dependent pathway, respectively. However, whether oltipraz also has an effect on immune cells, especially on T helper cell differentiation has to be elucidated. Here, we found that addition of oltipraz significantly inhibited Th2 differentiation under neutral and Th2-polarizing conditions while there was little, if any, effect on Th1 differentiation. In addition, TGF-{beta}-mediated Foxp3 induction in naïve CD4+ T cells was considerably reduced in the presence of oltipraz. Furthermore, Foxp3 induction was inhibited by oltipraz even in IFN-{gamma}-deficient naïve CD4+ T cells, indicating that oltipraz can inhibit TGF-{beta}-mediated Foxp3+ regulatory T cell differentiation through an IFN-{gamma}-independent manner. Therefore, these results suggest that oltipraz can act as an immune-modulating agent.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.184.Supp.139.15
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2010
    detail.hit.zdb_id: 1475085-5
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  • 9
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    Online Resource
    Peripheral Generation of CD4 + CD25 + Foxp3 + Regulatory T Cells
    XMLink ; 2007
    In:  Immune Network Vol. 7, No. 1 ( 2007), p. 1-
    Details
    In: Immune Network, XMLink, Vol. 7, No. 1 ( 2007), p. 1-
    Type of Medium: Online Resource
    ISSN: 1598-2629 , 2092-6685
    URL: Article
    DOI: 10.4110/in.2007.7.1.1
    Language: English
    Publisher: XMLink
    Publication Date: 2007
    detail.hit.zdb_id: 2536191-0
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  • 10
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    Online Resource
    Tumor-Derived Osteopontin Suppresses Antitumor Immunity by Promoting Extramedullary Myelopoiesis
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 22 ( 2014-11-15), p. 6705-6716
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 22 ( 2014-11-15), p. 6705-6716
    Abstract: Extramedullary myelopoiesis occurs commonly in tumor-bearing animals and is known to lead to accumulation of peripheral myeloid-derived suppressor cells (MDSC), which play an important role in immune escape. However, the cellular and molecular mechanisms by which tumors induce extramedullary myelopoiesis are poorly understood. In this study, we found that osteopontin expressed by tumor cells enhances extramedullary myelopoiesis in a CD44-dependent manner through the Erk1/2–MAPK pathway. Osteopontin-mediated extramedullary myelopoiesis was directly associated with increased MDSCs in tumor-bearing hosts. More importantly, osteopontin silencing in tumor cells delayed both tumor growth and extramedullary myelopoiesis, while the same treatment did not affect tumor growth in vitro. Finally, treatment with an antibody against osteopontin inhibited tumor growth and synergized with cell-based immunotherapeutic vaccines in mediating antitumor immunity. Our findings unveil a novel immunosuppressive role for tumor-derived osteopontin and offer a rationale for its therapeutic targeting in cancer treatment. Cancer Res; 74(22); 6705–16. ©2014 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-14-1482
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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