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  1. Article ; Online: Fatty acid oxidation fuels natural killer cell responses against infection and cancer.

    Sheppard, Sam / Srpan, Katja / Lin, Wendy / Lee, Mariah / Delconte, Rebecca B / Owyong, Mark / Carmeliet, Peter / Davis, Daniel M / Xavier, Joao B / Hsu, Katharine C / Sun, Joseph C

    Proceedings of the National Academy of Sciences of the United States of America

    2024  Volume 121, Issue 11, Page(s) e2319254121

    Abstract: Natural killer (NK) cells are a vital part of the innate immune system capable of rapidly clearing mutated or infected cells from the body and promoting an immune response. Here, we find that NK cells activated by viral infection or tumor challenge ... ...

    Abstract Natural killer (NK) cells are a vital part of the innate immune system capable of rapidly clearing mutated or infected cells from the body and promoting an immune response. Here, we find that NK cells activated by viral infection or tumor challenge increase uptake of fatty acids and their expression of carnitine palmitoyltransferase I (CPT1A), a critical enzyme for long-chain fatty acid oxidation. Using a mouse model with an NK cell-specific deletion of CPT1A, combined with stable
    MeSH term(s) Humans ; Lipid Metabolism ; Killer Cells, Natural ; Neoplasms ; Fatty Acids ; Virus Diseases
    Chemical Substances Fatty Acids
    Language English
    Publishing date 2024-03-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2319254121
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Cytotoxic lymphocytes target characteristic biophysical vulnerabilities in cancer.

    Tello-Lafoz, Maria / Srpan, Katja / Sanchez, Elisa E / Hu, Jing / Remsik, Jan / Romin, Yevgeniy / Calò, Annalisa / Hoen, Douglas / Bhanot, Umeshkumar / Morris, Luc / Boire, Adrienne / Hsu, Katharine C / Massagué, Joan / Huse, Morgan / Er, Ekrem Emrah

    Immunity

    2021  Volume 54, Issue 5, Page(s) 1037–1054.e7

    Abstract: Immune cells identify and destroy tumors by recognizing cellular traits indicative of oncogenic transformation. In this study, we found that myocardin-related transcription factors (MRTFs), which promote migration and metastatic invasion, also sensitize ... ...

    Abstract Immune cells identify and destroy tumors by recognizing cellular traits indicative of oncogenic transformation. In this study, we found that myocardin-related transcription factors (MRTFs), which promote migration and metastatic invasion, also sensitize cancer cells to the immune system. Melanoma and breast cancer cells with high MRTF expression were selectively eliminated by cytotoxic lymphocytes in mouse models of metastasis. This immunosurveillance phenotype was further enhanced by treatment with immune checkpoint blockade (ICB) antibodies. We also observed that high MRTF signaling in human melanoma is associated with ICB efficacy in patients. Using biophysical and functional assays, we showed that MRTF overexpression rigidified the filamentous actin cytoskeleton and that this mechanical change rendered mouse and human cancer cells more vulnerable to cytotoxic T lymphocytes and natural killer cells. Collectively, these results suggest that immunosurveillance has a mechanical dimension, which we call mechanosurveillance, that is particularly relevant for the targeting of metastatic disease.
    MeSH term(s) Actin Cytoskeleton/immunology ; Actins/immunology ; Animals ; Cell Communication/immunology ; Cell Line ; Cell Line, Tumor ; Cell Movement/immunology ; Female ; HEK293 Cells ; Humans ; Killer Cells, Natural/immunology ; Lymphocytes/immunology ; MCF-7 Cells ; Male ; Mice ; Mice, Inbred C57BL ; Neoplasms/immunology ; Signal Transduction/immunology ; Transcription Factors/immunology
    Chemical Substances Actins ; Transcription Factors
    Language English
    Publishing date 2021-03-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2021.02.020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4227: Show issues Location:
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    Zs.MG 69: Show issues

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  3. Article ; Online: Human Cytomegalovirus Infection Promotes Expansion of a Functionally Superior Cytoplasmic CD3

    Wu, Zeguang / Lau, Colleen M / Sottile, Rosa / Le Luduec, Jean-Benoît / Panjwani, M Kazim / Conaty, Peter M / Srpan, Katja / Laib Sampaio, Kerstin / Mertens, Thomas / Adler, Stuart P / Hill, Ann B / Barker, Juliet N / Cheung, Nai-Kong V / Sun, Joseph C / Hsu, Katharine C

    Journal of immunology (Baltimore, Md. : 1950)

    2021  Volume 207, Issue 10, Page(s) 2534–2544

    Abstract: Human CMV (HCMV) is a ubiquitous pathogen that indelibly shapes the NK cell repertoire. Using transcriptomic, epigenomic, and proteomic approaches to evaluate peripheral blood NK cells from healthy human volunteers, we find that prior HCMV infection ... ...

    Abstract Human CMV (HCMV) is a ubiquitous pathogen that indelibly shapes the NK cell repertoire. Using transcriptomic, epigenomic, and proteomic approaches to evaluate peripheral blood NK cells from healthy human volunteers, we find that prior HCMV infection promotes NK cells with a T cell-like gene profile, including the canonical markers CD3ε, CD5, and CD8β, as well as the T cell lineage-commitment transcription factor Bcl11b. Although Bcl11b expression is upregulated during NK maturation from CD56
    MeSH term(s) Animals ; Antibody-Dependent Cell Cytotoxicity/immunology ; CD3 Complex/immunology ; Cytomegalovirus Infections/immunology ; Humans ; Killer Cells, Natural/immunology ; Lymphocyte Subsets/immunology ; Mice ; Mice, Transgenic ; Repressor Proteins/immunology ; Transcriptome ; Tumor Suppressor Proteins/immunology
    Chemical Substances BCL11B protein, human ; CD3 Complex ; Repressor Proteins ; Tumor Suppressor Proteins
    Language English
    Publishing date 2021-10-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    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.2001319
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ud II Zs.37: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 28: Show issues

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  4. Article ; Online: Tunneling nanotube-mediated intercellular vesicle and protein transfer in the stroma-provided imatinib resistance in chronic myeloid leukemia cells.

    Kolba, Marta D / Dudka, Wioleta / Zaręba-Kozioł, Monika / Kominek, Agata / Ronchi, Paolo / Turos, Laura / Chroscicki, Piotr / Wlodarczyk, Jakub / Schwab, Yannick / Klejman, Agata / Cysewski, Dominik / Srpan, Katja / Davis, Daniel M / Piwocka, Katarzyna

    Cell death & disease

    2019  Volume 10, Issue 11, Page(s) 817

    Abstract: Intercellular communication within the bone marrow niche significantly promotes leukemogenesis and provides protection of leukemic cells from therapy. Secreted factors, intercellular transfer of mitochondria and the receptor-ligand interactions have been ...

    Abstract Intercellular communication within the bone marrow niche significantly promotes leukemogenesis and provides protection of leukemic cells from therapy. Secreted factors, intercellular transfer of mitochondria and the receptor-ligand interactions have been shown as mediators of this protection. Here we report that tunneling nanotubes (TNTs)-long, thin membranous structures, which have been identified as a novel mode of intercellular cross-talk-are formed in the presence of stroma and mediate transfer of cellular vesicles from stroma to leukemic cells. Importantly, transmission of vesicles via TNTs from stromal cells increases resistance of leukemic cells to the tyrosine kinase inhibitor, imatinib. Using correlative light-electron microscopy and electron tomography we show that stromal TNTs contain vesicles, provide membrane continuity with the cell bodies and can be open-ended. Moreover, trans-SILAC studies to reveal the non-autonomous proteome showed that specific sets of proteins are transferred together with cellular vesicles from stromal to leukemic cells, with a potential role in survival and adaptation. Altogether, our findings provide evidence for the biological role of the TNT-mediated vesicle exchange between stromal and leukemic cells, implicating the direct vesicle and protein transfer in the stroma-provided protection of leukemic cells.
    MeSH term(s) Biological Transport/genetics ; Cell Communication/drug effects ; Cell Line, Tumor ; Drug Resistance, Neoplasm/genetics ; Humans ; Imatinib Mesylate/chemistry ; Imatinib Mesylate/pharmacology ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/pathology ; Microscopy, Electron ; Mitochondria/drug effects ; Mitochondria/genetics ; Nanotubes/chemistry ; Stromal Cells/drug effects ; Stromal Cells/ultrastructure
    Chemical Substances Imatinib Mesylate (8A1O1M485B)
    Language English
    Publishing date 2019-10-28
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-019-2045-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Shedding of CD16 disassembles the NK cell immune synapse and boosts serial engagement of target cells.

    Srpan, Katja / Ambrose, Ashley / Karampatzakis, Alexandros / Saeed, Mezida / Cartwright, Adam N R / Guldevall, Karolin / De Matos, Gabriela Dos Santos Cruz / Önfelt, Björn / Davis, Daniel M

    The Journal of cell biology

    2018  Volume 217, Issue 9, Page(s) 3267–3283

    Abstract: Natural Killer (NK) cells can engage multiple virally infected or tumor cells sequentially and deliver perforin for cytolytic killing of these targets. Using microscopy to visualize degranulation from individual NK cells, we found that repeated ... ...

    Abstract Natural Killer (NK) cells can engage multiple virally infected or tumor cells sequentially and deliver perforin for cytolytic killing of these targets. Using microscopy to visualize degranulation from individual NK cells, we found that repeated activation via the Fc receptor CD16 decreased the amount of perforin secreted. However, perforin secretion was restored upon subsequent activation via a different activating receptor, NKG2D. Repeated stimulation via NKG2D also decreased perforin secretion, but this was not rescued by stimulation via CD16. These different outcomes of sequential stimulation could be accounted for by shedding of CD16 being triggered by cellular activation. The use of pharmacological inhibitors and NK cells transfected to express a noncleavable form of CD16 revealed that CD16 shedding also increased NK cell motility and facilitated detachment of NK cells from target cells. Disassembly of the immune synapse caused by CD16 shedding aided NK cell survival and boosted serial engagement of target cells. Thus, counterintuitively, shedding of CD16 may positively impact immune responses.
    MeSH term(s) Antineoplastic Agents, Immunological/pharmacology ; Cell Degranulation/immunology ; Cell Line, Tumor ; Cell Movement/immunology ; Cytotoxicity, Immunologic/immunology ; GPI-Linked Proteins/genetics ; GPI-Linked Proteins/metabolism ; Humans ; Killer Cells, Natural/cytology ; Killer Cells, Natural/immunology ; Lymphocyte Activation/immunology ; NK Cell Lectin-Like Receptor Subfamily K/metabolism ; Neoplasms/immunology ; Perforin/metabolism ; Receptors, IgG/genetics ; Receptors, IgG/metabolism ; Rituximab/pharmacology
    Chemical Substances Antineoplastic Agents, Immunological ; FCGR3B protein, human ; GPI-Linked Proteins ; KLRK1 protein, human ; NK Cell Lectin-Like Receptor Subfamily K ; Receptors, IgG ; Perforin (126465-35-8) ; Rituximab (4F4X42SYQ6)
    Language English
    Publishing date 2018-07-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.201712085
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ub I Zs.190: Show issues Location:
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