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  1. Article ; Online: IL-23 stabilizes an effector T

    Wertheimer, Tobias / Zwicky, Pascale / Rindlisbacher, Lukas / Sparano, Colin / Vermeer, Marijne / de Melo, Bruno Marcel Silva / Haftmann, Claudia / Rückert, Tamina / Sethi, Aakriti / Schärli, Stefanie / Huber, Anna / Ingelfinger, Florian / Xu, Caroline / Kim, Daehong / Häne, Philipp / Fonseca da Silva, André / Muschaweckh, Andreas / Nunez, Nicolas / Krishnarajah, Sinduya /
    Köhler, Natalie / Zeiser, Robert / Oukka, Mohamed / Korn, Thomas / Tugues, Sonia / Becher, Burkhard

    Nature immunology

    2024  Volume 25, Issue 3, Page(s) 512–524

    Abstract: Interleukin-23 (IL-23) is a proinflammatory cytokine mainly produced by myeloid cells that promotes tumor growth in various preclinical cancer models and correlates with adverse outcomes. However, as to how IL-23 fuels tumor growth is unclear. Here, we ... ...

    Abstract Interleukin-23 (IL-23) is a proinflammatory cytokine mainly produced by myeloid cells that promotes tumor growth in various preclinical cancer models and correlates with adverse outcomes. However, as to how IL-23 fuels tumor growth is unclear. Here, we found tumor-associated macrophages to be the main source of IL-23 in mouse and human tumor microenvironments. Among IL-23-sensing cells, we identified a subset of tumor-infiltrating regulatory T (T
    MeSH term(s) Animals ; Humans ; Mice ; Cytokines ; Interleukin-23/genetics ; Neoplasms/genetics ; T-Lymphocytes ; Tumor Microenvironment
    Chemical Substances Cytokines ; Interleukin-23
    Language English
    Publishing date 2024-02-14
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-024-01755-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5294: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 42: Show issues

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  2. Article ; Online: Azathioprine therapy induces selective NK cell depletion and IFN-γ deficiency predisposing to herpesvirus reactivation.

    Ingelfinger, Florian / Sparano, Colin / Bamert, David / Reyes-Leiva, David / Sethi, Aakriti / Rindlisbacher, Lukas / Zwicky, Pascale / Kreutmair, Stefanie / Widmer, Corinne C / Mundt, Sarah / Cortés-Vicente, Elena / Tugues, Sonia / Becher, Burkhard / Schreiner, Bettina

    The Journal of allergy and clinical immunology

    2022  Volume 151, Issue 1, Page(s) 280–286.e2

    Abstract: Background: Azathioprine is a widely prescribed drug for patients with chronic inflammatory diseases such as myasthenia gravis or organ transplant recipients. Azathioprine exerts immunosuppressive effects by inhibiting intracellular purine synthesis and ...

    Abstract Background: Azathioprine is a widely prescribed drug for patients with chronic inflammatory diseases such as myasthenia gravis or organ transplant recipients. Azathioprine exerts immunosuppressive effects by inhibiting intracellular purine synthesis and reducing the numbers of circulating B and T lymphocytes. Case reports indicate increased risk for serious infections that can occur despite regular measurements of lymphocyte counts during azathioprine therapy.
    Objective: We sought to comprehensively investigate therapy-associated patient risks and the underlying immune dysfunction of azathioprine use.
    Methods: Peripheral blood leukocytes were analyzed using single-cell mass and spectral flow cytometry to detect specific effects of azathioprine use on the systemic immune signature. Therapy-associated clinical features were analyzed in 2 independent cohorts of myasthenia gravis patients.
    Results: Azathioprine therapy selectively induced pronounced CD56
    Conclusion: Our study highlights the risk of development of adverse events during azathioprine therapy and suggests that natural killer cell monitoring could be valuable in clinical practice.
    MeSH term(s) Humans ; Azathioprine/adverse effects ; Killer Cells, Natural ; Interferon-gamma/pharmacology ; Herpesviridae ; Myasthenia Gravis/drug therapy ; Myasthenia Gravis/chemically induced
    Chemical Substances Azathioprine (MRK240IY2L) ; Interferon-gamma (82115-62-6)
    Language English
    Publishing date 2022-09-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2022.09.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Embryonic and neonatal waves generate distinct populations of hepatic ILC1s.

    Sparano, Colin / Solís-Sayago, Darío / Vijaykumar, Anjali / Rickenbach, Chiara / Vermeer, Marijne / Ingelfinger, Florian / Litscher, Gioana / Fonseca, André / Mussak, Caroline / Mayoux, Maud / Friedrich, Christin / Nombela-Arrieta, César / Gasteiger, Georg / Becher, Burkhard / Tugues, Sonia

    Science immunology

    2022  Volume 7, Issue 75, Page(s) eabo6641

    Abstract: Group 1 innate lymphoid cells (ILCs) comprising circulating natural killer (cNK) cells and tissue-resident ILC1s are critical for host defense against pathogens and tumors. Despite a growing understanding of their role in homeostasis and disease, the ... ...

    Abstract Group 1 innate lymphoid cells (ILCs) comprising circulating natural killer (cNK) cells and tissue-resident ILC1s are critical for host defense against pathogens and tumors. Despite a growing understanding of their role in homeostasis and disease, the ontogeny of group 1 ILCs remains largely unknown. Here, we used fate mapping and single-cell transcriptomics to comprehensively investigate the origin and turnover of murine group 1 ILCs. Whereas cNK cells are continuously replaced throughout life, we uncovered tissue-dependent development and turnover of ILC1s. A first wave of ILC1s emerges during embryogenesis in the liver and transiently colonizes fetal tissues. After birth, a second wave quickly replaces ILC1s in most tissues apart from the liver, where they layer with embryonic ILC1s, persist until adulthood, and undergo a specific developmental program. Whereas embryonically derived ILC1s give rise to a cytotoxic subset, the neonatal wave establishes the full spectrum of ILC1s. Our findings uncover key ontogenic features of murine group 1 ILCs and their association with cellular identities and functions.
    MeSH term(s) Animals ; Fetus ; Immunity, Innate ; Killer Cells, Natural ; Liver ; Mice
    Language English
    Publishing date 2022-09-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2470-9468
    ISSN (online) 2470-9468
    DOI 10.1126/sciimmunol.abo6641
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: NKG2D-mediated detection of metabolically stressed hepatocytes by innate-like T cells is essential for initiation of NASH and fibrosis.

    Marinović, Sonja / Lenartić, Maja / Mladenić, Karlo / Šestan, Marko / Kavazović, Inga / Benić, Ante / Krapić, Mia / Rindlisbacher, Lukas / Cokarić Brdovčak, Maja / Sparano, Colin / Litscher, Gioana / Turk Wensveen, Tamara / Mikolašević, Ivana / Fučkar Čupić, Dora / Bilić-Zulle, Lidija / Steinle, Aleksander / Waisman, Ari / Hayday, Adrian / Tugues, Sonia /
    Becher, Burkhard / Polić, Bojan / Wensveen, Felix M

    Science immunology

    2023  Volume 8, Issue 87, Page(s) eadd1599

    Abstract: Metabolic-associated fatty liver disease (MAFLD) is a spectrum of clinical manifestations ranging from benign steatosis to cirrhosis. A key event in the pathophysiology of MAFLD is the development of nonalcoholic steatohepatitis (NASH), which can ... ...

    Abstract Metabolic-associated fatty liver disease (MAFLD) is a spectrum of clinical manifestations ranging from benign steatosis to cirrhosis. A key event in the pathophysiology of MAFLD is the development of nonalcoholic steatohepatitis (NASH), which can potentially lead to fibrosis and hepatocellular carcinoma, but the triggers of MAFLD-associated inflammation are not well understood. We have observed that lipid accumulation in hepatocytes induces expression of ligands specific to the activating immune receptor NKG2D. Tissue-resident innate-like T cells, most notably γδ T cells, are activated through NKG2D and secrete IL-17A. IL-17A licenses hepatocytes to produce chemokines that recruit proinflammatory cells into the liver, which causes NASH and fibrosis. NKG2D-deficient mice did not develop fibrosis in dietary models of NASH and had a decreased incidence of hepatic tumors. The frequency of IL-17A
    MeSH term(s) Animals ; Humans ; Mice ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Inflammation/pathology ; Interleukin-17/metabolism ; Liver Cirrhosis/metabolism ; NK Cell Lectin-Like Receptor Subfamily K ; Non-alcoholic Fatty Liver Disease ; T-Lymphocytes/metabolism
    Chemical Substances Interleukin-17 ; NK Cell Lectin-Like Receptor Subfamily K ; Klrk1 protein, mouse
    Language English
    Publishing date 2023-09-29
    Publishing country United States
    Document type Journal Article
    ISSN 2470-9468
    ISSN (online) 2470-9468
    DOI 10.1126/sciimmunol.add1599
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Cancer-Cell-Intrinsic cGAS Expression Mediates Tumor Immunogenicity.

    Schadt, Linda / Sparano, Colin / Schweiger, Nicole Angelika / Silina, Karina / Cecconi, Virginia / Lucchiari, Giulia / Yagita, Hideo / Guggisberg, Emilien / Saba, Sascha / Nascakova, Zuzana / Barchet, Winfried / van den Broek, Maries

    Cell reports

    2019  Volume 29, Issue 5, Page(s) 1236–1248.e7

    Abstract: Sensing of cytoplasmic DNA by cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) synthase (cGAS) results in production of the dinucleotide cGAMP and consecutive activation of stimulator of interferon genes (STING) followed by production of ... ...

    Abstract Sensing of cytoplasmic DNA by cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) synthase (cGAS) results in production of the dinucleotide cGAMP and consecutive activation of stimulator of interferon genes (STING) followed by production of type I interferon (IFN). Although cancer cells contain supra-normal concentrations of cytoplasmic DNA, they rarely produce type I IFN spontaneously. This suggests that defects in the DNA-sensing pathway may serve as an immune escape mechanism. We find that cancer cells produce cGAMP that is transferred via gap junctions to tumor-associated dendritic cells (DCs) and macrophages, which respond by producing type I IFN in situ. Cancer-cell-intrinsic expression of cGAS, but not STING, promotes infiltration by effector CD8
    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes/immunology ; Cell Line, Tumor ; DNA Damage ; Dendritic Cells/metabolism ; Disease Progression ; Humans ; Immunotherapy ; Interferon Type I/metabolism ; Membrane Proteins ; Mice, Inbred C57BL ; Microsatellite Repeats/genetics ; Neoplasms/drug therapy ; Neoplasms/immunology ; Neoplasms/pathology ; Nucleotides, Cyclic/metabolism ; Nucleotidyltransferases/metabolism
    Chemical Substances Interferon Type I ; Membrane Proteins ; Nucleotides, Cyclic ; Sting1 protein, mouse ; cyclic guanosine monophosphate-adenosine monophosphate ; Nucleotidyltransferases (EC 2.7.7.-) ; cGAS protein, human (EC 2.7.7.-) ; cGAS protein, mouse (EC 2.7.7.-)
    Language English
    Publishing date 2019-10-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2019.09.065
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Single-cell profiling of immune system alterations in lymphoid, barrier and solid tissues in aged mice.

    Krishnarajah, Sinduya / Ingelfinger, Florian / Friebel, Ekaterina / Cansever, Dilay / Amorim, Ana / Andreadou, Myrto / Bamert, David / Litscher, Gioana / Lutz, Mirjam / Mayoux, Maud / Mundt, Sarah / Ridder, Frederike / Sparano, Colin / Stifter, Sebastian Anton / Ulutekin, Can / Unger, Susanne / Vermeer, Marijne / Zwicky, Pascale / Greter, Melanie /
    Tugues, Sonia / De Feo, Donatella / Becher, Burkhard

    Nature aging

    2021  Volume 2, Issue 1, Page(s) 74–89

    Abstract: Aging exerts profound and paradoxical effects on the immune system, at once impairing proliferation, cytotoxicity and phagocytosis, and inducing chronic inflammation. Previous studies have focused on individual tissues or cell types, while a ... ...

    Abstract Aging exerts profound and paradoxical effects on the immune system, at once impairing proliferation, cytotoxicity and phagocytosis, and inducing chronic inflammation. Previous studies have focused on individual tissues or cell types, while a comprehensive multisystem study of tissue-resident and circulating immune populations during aging is lacking. Here we reveal an atlas of age-related changes in the abundance and phenotype of immune cell populations across 12 mouse tissues. Using cytometry-based high parametric analysis of 37 mass-cytometry and 55 spectral flow-cytometry parameters, mapping samples from young and aged animals revealed conserved and tissue-type-specific patterns of both immune atrophy and expansion. We uncovered clear phenotypic changes in both lymphoid and myeloid lineages in aged mice, and in particular a contraction in natural killer cells and plasmacytoid dendritic cells. These changes correlated with a skewing towards myelopoiesis at the expense of early lymphocyte genesis in aged mice. Taken together, this atlas represents a comprehensive, systematic and thorough resource of the age-dependent alterations of the mammalian immune system in lymphoid, barrier and solid tissues.
    MeSH term(s) Mice ; Animals ; Flow Cytometry ; Killer Cells, Natural ; Phagocytosis ; Inflammation ; Phenotype ; Mammals
    Language English
    Publishing date 2021-12-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2662-8465
    ISSN (online) 2662-8465
    DOI 10.1038/s43587-021-00148-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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