Search Results - (Author, Cooperation:P. S. Ohashi)
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1Latest Papers from Table of Contents or Articles in PressD. R. McIlwain ; P. A. Lang ; T. Maretzky ; K. Hamada ; K. Ohishi ; S. K. Maney ; T. Berger ; A. Murthy ; G. Duncan ; H. C. Xu ; K. S. Lang ; D. Haussinger ; A. Wakeham ; A. Itie-Youten ; R. Khokha ; P. S. Ohashi ; C. P. Blobel ; T. W. Mak
American Association for the Advancement of Science (AAAS)
Published 2012Staff ViewPublication Date: 2012-01-17Publisher: American Association for the Advancement of Science (AAAS)Print ISSN: 0036-8075Electronic ISSN: 1095-9203Topics: BiologyChemistry and PharmacologyComputer ScienceMedicineNatural Sciences in GeneralPhysicsKeywords: ADAM Proteins/genetics/*metabolism ; Amino Acid Sequence ; Animals ; B-Lymphocytes/immunology/metabolism ; Base Sequence ; Carrier Proteins/chemistry/genetics/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Gene Deletion ; *Immunity, Innate ; Lipopolysaccharides/*immunology ; Listeria monocytogenes/immunology/physiology ; Listeriosis/*immunology/metabolism/microbiology/pathology ; Macrophages/immunology/metabolism ; Macrophages, Peritoneal/immunology/metabolism/microbiology ; Mice ; Molecular Sequence Data ; Protein Transport ; Shock, Septic/*immunology/metabolism ; Spleen/cytology ; Tumor Necrosis Factor-alpha/blood/genetics/*metabolismPublished by: -
2Latest Papers from Table of Contents or Articles in PressM. Sasaki ; C. B. Knobbe ; J. C. Munger ; E. F. Lind ; D. Brenner ; A. Brustle ; I. S. Harris ; R. Holmes ; A. Wakeham ; J. Haight ; A. You-Ten ; W. Y. Li ; S. Schalm ; S. M. Su ; C. Virtanen ; G. Reifenberger ; P. S. Ohashi ; D. L. Barber ; M. E. Figueroa ; A. Melnick ; J. C. Zuniga-Pflucker ; T. W. Mak
Nature Publishing Group (NPG)
Published 2012Staff ViewPublication Date: 2012-07-06Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Aging ; Animals ; Bone Marrow/pathology ; Cell Lineage ; CpG Islands/genetics ; DNA Methylation ; Disease Models, Animal ; Epigenesis, Genetic/*genetics ; Female ; Gene Knock-In Techniques ; Glioma/pathology ; Hematopoiesis ; Hematopoietic Stem Cells/*cytology/metabolism ; Histones/metabolism ; Humans ; Isocitrate Dehydrogenase/*genetics/*metabolism ; Leukemia, Myeloid, Acute/genetics ; Male ; Mice ; Mutant Proteins/genetics/*metabolism ; Mutation/*genetics ; Myeloid Cells/cytology/metabolism ; Spleen/pathologyPublished by: -
3Latest Papers from Table of Contents or Articles in PressToker, A., Nguyen, L. T., Stone, S. C., Yang, S. Y. C., Katz, S. R., Shaw, P. A., Clarke, B. A., Ghazarian, D., Al-Habeeb, A., Easson, A., Leong, W. L., McCready, D. R., Reedijk, M., Guidos, C. J., Pugh, T. J., Bernardini, M. Q., Ohashi, P. S.
The American Association for Cancer Research (AACR)
Published 2018Staff ViewPublication Date: 2018-11-16Publisher: The American Association for Cancer Research (AACR)Print ISSN: 1078-0432Electronic ISSN: 1557-3265Topics: MedicinePublished by: -
4Articles: DFG German National LicensesStaff View
ISSN: 1420-9071Keywords: Key words. Acute autoimmunity; chronic autoimmune disease; CTL; immunotherapy; tumour antigen; tumour immunogenicity.Source: Springer Online Journal Archives 1860-2000Topics: BiologyMedicineNotes: Abstract. Tumour-specific cytotoxic T cells (CTLs) are among the best-defined biological anticancer weapons. Nevertheless, they often fail to control tumour growth in vivo. Many reasons for this have been evoked tumours may actively inhibit CTLs, or may protect them selves from CTL recognition by various means. However, one does not necessarily need to postulate such active immune evasion mechanisms specifically acquired by tumour cells. In this review we argue that the failure of immune protection is due to the intrinsic inability of tumours to activate an effective immune response, and that many tumours are similar to normal issues in this respect. It is striking to see that the majority of the so-called immune escape mechanisms are not specifically acquired by selected tumour cells, but are common mechanisms shared between solid tumours and normal, healthy tissues. Immune responses are poor because tumour antigens do not efficiently localize to lymph follicles in lymphoid tissues, and are not efficiently presented to CTLs in an immunogenic context. The fact that tumours do not induce CTLs but are often susceptible to lymphocyte-mediated cytotoxicity indicates that more intensified immunization protocols should result in improved clinical outcome.Type of Medium: Electronic ResourceURL: