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  • 1
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    Granzyme M has a critical role in providing innate immune protection in ulcerative colitis (2016)
    Springer Nature
    Details
    Publication Date: 2016-07-22
    Description: Granzyme M has a critical role in providing innate immune protection in ulcerative colitis Cell Death and Disease 7, e2302 (July 2016). doi:10.1038/cddis.2016.215 Authors: F Souza-Fonseca-Guimaraes, Y Krasnova, T Putoczki, K Miles, K P MacDonald, L Town, W Shi, G C Gobe, L McDade, L A Mielke, H Tye, S L Masters, G T Belz, N D Huntington, G Radford-Smith & M J Smyth
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 2
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    NK cell intrinsic regulation of MIP-1α by granzyme M (2014)
    Springer Nature
    Details
    Publication Date: 2014-03-14
    Description: NK cell intrinsic regulation of MIP-1α by granzyme M Cell Death and Disease 5, e1115 (March 2014). doi:10.1038/cddis.2014.74 Authors: N Baschuk, N Wang, S V Watt, H Halse, C House, P I Bird, R Strugnell, J A Trapani, M J Smyth & D M Andrews
    Keywords: NK cellsGranzyme MMIP-1αListeria monocytogenes infection
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 3
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    Membrane-bound Fas ligand only is essential for Fas-induced apoptosis (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-10-02
    Description: Fas ligand (FasL), an apoptosis-inducing member of the TNF cytokine family, and its receptor Fas are critical for the shutdown of chronic immune responses and prevention of autoimmunity. Accordingly, mutations in their genes cause severe lymphadenopathy and autoimmune disease in mice and humans. FasL function is regulated by deposition in the plasma membrane and metalloprotease-mediated shedding. Here we generated gene-targeted mice that selectively lack either secreted FasL (sFasL) or membrane-bound FasL (mFasL) to resolve which of these forms is required for cell killing and to explore their hypothesized non-apoptotic activities. Mice lacking sFasL (FasL(Deltas/Deltas)) appeared normal and their T cells readily killed target cells, whereas T cells lacking mFasL (FasL(Deltam/Deltam)) could not kill cells through Fas activation. FasL(Deltam/Deltam) mice developed lymphadenopathy and hyper-gammaglobulinaemia, similar to FasL(gld/gld) mice, which express a mutant form of FasL that cannot bind Fas, but surprisingly, FasL(Deltam/Deltam) mice (on a C57BL/6 background) succumbed to systemic lupus erythematosus (SLE)-like autoimmune kidney destruction and histiocytic sarcoma, diseases that occur only rarely and much later in FasL(gld/gld) mice. These results demonstrate that mFasL is essential for cytotoxic activity and constitutes the guardian against lymphadenopathy, autoimmunity and cancer, whereas excess sFasL appears to promote autoimmunity and tumorigenesis through non-apoptotic activities.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2785124/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2785124/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O' Reilly, Lorraine A -- Tai, Lin -- Lee, Lily -- Kruse, Elizabeth A -- Grabow, Stephanie -- Fairlie, W Douglas -- Haynes, Nicole M -- Tarlinton, David M -- Zhang, Jian-Guo -- Belz, Gabrielle T -- Smyth, Mark J -- Bouillet, Philippe -- Robb, Lorraine -- Strasser, Andreas -- CA043540-18/CA/NCI NIH HHS/ -- CA80188-6/CA/NCI NIH HHS/ -- R01 CA043540/CA/NCI NIH HHS/ -- R01 CA043540-18/CA/NCI NIH HHS/ -- R01 CA080188-06/CA/NCI NIH HHS/ -- England -- Nature. 2009 Oct 1;461(7264):659-63. doi: 10.1038/nature08402.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19794494" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Antinuclear/immunology ; Antigens, CD95/*metabolism ; *Apoptosis ; Cell Membrane/*metabolism ; Cytidine Deaminase/metabolism ; Cytotoxicity, Immunologic ; Fas Ligand Protein/deficiency/genetics/*metabolism/secretion ; Glomerulonephritis/metabolism ; Histiocytic Sarcoma/metabolism ; Hypergammaglobulinemia/metabolism ; Lupus Erythematosus, Systemic/metabolism ; Lymphatic Diseases/metabolism ; Mice ; Mice, Inbred C57BL ; Mutation ; Splenomegaly/metabolism ; T-Lymphocytes/immunology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Immunology. Making macrophages eat cancer (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-07-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kershaw, Michael H -- Smyth, Mark J -- New York, N.Y. -- Science. 2013 Jul 5;341(6141):41-2. doi: 10.1126/science.1241716.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Immunology Program, Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, 3010 Victoria, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23828933" target="_blank"〉PubMed〈/a〉
    Keywords: *Adjuvants, Immunologic ; Animals ; Antibodies, Monoclonal/*therapeutic use ; Antibodies, Neoplasm/*therapeutic use ; Antigens, CD47/*immunology ; Antigens, Differentiation/*therapeutic use ; Humans ; Neoplasms/*therapy ; Receptors, Immunologic/*therapeutic use
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Immunology. The elusive NKT cell antigen--is the search over? (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Godfrey, Dale I -- Pellicci, Daniel G -- Smyth, Mark J -- New York, N.Y. -- Science. 2004 Dec 3;306(5702):1687-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of Melbourne, Melbourne, Victoria, Australia. godfrey@unimelb.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15576595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD1/immunology ; Antigens, CD1d ; Carbohydrate Conformation ; Galactosyltransferases/genetics/metabolism ; Globosides/*immunology/metabolism ; Humans ; Immune Tolerance ; Killer Cells, Natural/*immunology ; Ligands ; Lymphocyte Activation ; Lysosomes/metabolism ; Mice ; T-Lymphocyte Subsets/*immunology ; Thymus Gland/immunology ; beta-N-Acetylhexosaminidases/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    Cancer exome analysis reveals a T-cell-dependent mechanism of cancer immunoediting (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-02-10
    Description: Cancer immunoediting, the process by which the immune system controls tumour outgrowth and shapes tumour immunogenicity, is comprised of three phases: elimination, equilibrium and escape. Although many immune components that participate in this process are known, its underlying mechanisms remain poorly defined. A central tenet of cancer immunoediting is that T-cell recognition of tumour antigens drives the immunological destruction or sculpting of a developing cancer. However, our current understanding of tumour antigens comes largely from analyses of cancers that develop in immunocompetent hosts and thus may have already been edited. Little is known about the antigens expressed in nascent tumour cells, whether they are sufficient to induce protective antitumour immune responses or whether their expression is modulated by the immune system. Here, using massively parallel sequencing, we characterize expressed mutations in highly immunogenic methylcholanthrene-induced sarcomas derived from immunodeficient Rag2(-/-) mice that phenotypically resemble nascent primary tumour cells. Using class I prediction algorithms, we identify mutant spectrin-beta2 as a potential rejection antigen of the d42m1 sarcoma and validate this prediction by conventional antigen expression cloning and detection. We also demonstrate that cancer immunoediting of d42m1 occurs via a T-cell-dependent immunoselection process that promotes outgrowth of pre-existing tumour cell clones lacking highly antigenic mutant spectrin-beta2 and other potential strong antigens. These results demonstrate that the strong immunogenicity of an unedited tumour can be ascribed to expression of highly antigenic mutant proteins and show that outgrowth of tumour cells that lack these strong antigens via a T-cell-dependent immunoselection process represents one mechanism of cancer immunoediting.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3874809/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3874809/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsushita, Hirokazu -- Vesely, Matthew D -- Koboldt, Daniel C -- Rickert, Charles G -- Uppaluri, Ravindra -- Magrini, Vincent J -- Arthur, Cora D -- White, J Michael -- Chen, Yee-Shiuan -- Shea, Lauren K -- Hundal, Jasreet -- Wendl, Michael C -- Demeter, Ryan -- Wylie, Todd -- Allison, James P -- Smyth, Mark J -- Old, Lloyd J -- Mardis, Elaine R -- Schreiber, Robert D -- R01 CA043059/CA/NCI NIH HHS/ -- U01 CA141541/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Feb 8;482(7385):400-4. doi: 10.1038/nature10755.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22318521" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Carrier Proteins/genetics/immunology ; DNA-Binding Proteins/deficiency/genetics ; Exome/*genetics/*immunology ; Histocompatibility Antigens Class I/immunology ; Humans ; Immunologic Surveillance/*immunology ; Male ; Methylcholanthrene ; Mice ; Microfilament Proteins/genetics/immunology ; Models, Immunological ; Neoplasms/chemically induced/*genetics/*immunology/pathology ; Reproducibility of Results ; Sarcoma/chemically induced/genetics/immunology/pathology ; T-Lymphocytes/*immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 7
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    Cancer immunoediting: integrating immunity's roles in cancer suppression and promotion (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-26
    Description: Understanding how the immune system affects cancer development and progression has been one of the most challenging questions in immunology. Research over the past two decades has helped explain why the answer to this question has evaded us for so long. We now appreciate that the immune system plays a dual role in cancer: It can not only suppress tumor growth by destroying cancer cells or inhibiting their outgrowth but also promote tumor progression either by selecting for tumor cells that are more fit to survive in an immunocompetent host or by establishing conditions within the tumor microenvironment that facilitate tumor outgrowth. Here, we discuss a unifying conceptual framework called "cancer immunoediting," which integrates the immune system's dual host-protective and tumor-promoting roles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schreiber, Robert D -- Old, Lloyd J -- Smyth, Mark J -- New York, N.Y. -- Science. 2011 Mar 25;331(6024):1565-70. doi: 10.1126/science.1203486.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. schreiber@immunology.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21436444" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Animals ; Antigens, Neoplasm/immunology ; Humans ; Immune System/*physiology ; Immune Tolerance ; Immunity, Innate ; Immunocompromised Host ; Immunologic Surveillance ; Immunotherapy ; Lymphocytes, Tumor-Infiltrating/immunology ; Mice ; Models, Immunological ; Neoplasms/*immunology/therapy ; Prognosis ; Tumor Escape
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 8
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    Immunology. The adjuvant effects of antibodies (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smyth, Mark J -- Kershaw, Michael H -- New York, N.Y. -- Science. 2011 Aug 19;333(6045):944-5. doi: 10.1126/science.1210801.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Immunology Program, Peter MacCallum Cancer Centre, East Melbourne, 3002 Victoria, Australia. mark.smyth@petermac.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21852479" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; *Adjuvants, Immunologic ; Animals ; Antibodies, Monoclonal/*immunology/metabolism ; Antigen Presentation ; Antigen-Presenting Cells/immunology ; Antigens, CD40/*immunology ; Dendritic Cells/immunology ; Immunoglobulin Fc Fragments/immunology/metabolism ; Lymphocyte Activation ; Mice ; Neoplasms/immunology/therapy ; Ovalbumin/immunology ; Receptors, IgG/immunology/metabolism ; Signal Transduction ; T-Lymphocytes/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 9
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    An immunosurveillance mechanism controls cancer cell ploidy (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-29
    Description: Cancer cells accommodate multiple genetic and epigenetic alterations that initially activate intrinsic (cell-autonomous) and extrinsic (immune-mediated) oncosuppressive mechanisms. Only once these barriers to oncogenesis have been overcome can malignant growth proceed unrestrained. Tetraploidization can contribute to oncogenesis because hyperploid cells are genomically unstable. We report that hyperploid cancer cells become immunogenic because of a constitutive endoplasmic reticulum stress response resulting in the aberrant cell surface exposure of calreticulin. Hyperploid, calreticulin-exposing cancer cells readily proliferated in immunodeficient mice and conserved their increased DNA content. In contrast, hyperploid cells injected into immunocompetent mice generated tumors only after a delay, and such tumors exhibited reduced DNA content, endoplasmic reticulum stress, and calreticulin exposure. Our results unveil an immunosurveillance system that imposes immunoselection against hyperploidy in carcinogen- and oncogene-induced cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Senovilla, Laura -- Vitale, Ilio -- Martins, Isabelle -- Tailler, Maximilien -- Pailleret, Claire -- Michaud, Mickael -- Galluzzi, Lorenzo -- Adjemian, Sandy -- Kepp, Oliver -- Niso-Santano, Mireia -- Shen, Shensi -- Marino, Guillermo -- Criollo, Alfredo -- Boileve, Alice -- Job, Bastien -- Ladoire, Sylvain -- Ghiringhelli, Francois -- Sistigu, Antonella -- Yamazaki, Takahiro -- Rello-Varona, Santiago -- Locher, Clara -- Poirier-Colame, Vichnou -- Talbot, Monique -- Valent, Alexander -- Berardinelli, Francesco -- Antoccia, Antonio -- Ciccosanti, Fabiola -- Fimia, Gian Maria -- Piacentini, Mauro -- Fueyo, Antonio -- Messina, Nicole L -- Li, Ming -- Chan, Christopher J -- Sigl, Verena -- Pourcher, Guillaume -- Ruckenstuhl, Christoph -- Carmona-Gutierrez, Didac -- Lazar, Vladimir -- Penninger, Josef M -- Madeo, Frank -- Lopez-Otin, Carlos -- Smyth, Mark J -- Zitvogel, Laurence -- Castedo, Maria -- Kroemer, Guido -- New York, N.Y. -- Science. 2012 Sep 28;337(6102):1678-84.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM, U848, Villejuif, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23019653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calreticulin/immunology ; Cell Line, Tumor ; Common Variable Immunodeficiency/genetics ; DNA, Neoplasm/analysis/genetics ; Endoplasmic Reticulum Stress/*immunology ; Eukaryotic Initiation Factor-2/metabolism ; Humans ; Immunocompetence ; *Immunologic Surveillance ; Mice ; Mice, Inbred BALB C ; Neoplasms/chemically induced/*genetics/*immunology ; Phosphorylation ; *Ploidies
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 10
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    Cancer. Can cancer trigger autoimmunity? (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-01-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Teng, Michele W L -- Smyth, Mark J -- New York, N.Y. -- Science. 2014 Jan 10;343(6167):147-8. doi: 10.1126/science.1249486.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Immunoregulation and Immunotherapy and Immunology in Cancer and Infection Laboratories, QIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, 4006 Queensland, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24408426" target="_blank"〉PubMed〈/a〉
    Keywords: Autoantigens/*immunology ; Autoimmune Diseases/*complications ; Humans ; Neoplasms/*immunology ; RNA Polymerase III/*immunology ; Scleroderma, Systemic/*complications
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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