M
Maurizio Zanetti
Researcher at University of California, San Diego
Publications - 163
Citations - 4255
Maurizio Zanetti is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Antigen & Cytotoxic T cell. The author has an hindex of 35, co-authored 156 publications receiving 3787 citations. Previous affiliations of Maurizio Zanetti include University of California & University of California, Berkeley.
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Journal ArticleDOI
Cytotoxic T cell immunity against telomerase reverse transcriptase in humans.
Boris Minev,Jason D. Hipp,Hüseyin Firat,Joseph D. Schmidt,Pierre Langlade-Demoyen,Maurizio Zanetti +5 more
TL;DR: It is demonstrated here that the majority of normal individuals and patients with prostate cancer immunized in vitro against two HLA-A2.1 restricted peptides from telomerase reverse transcriptase (hTRT) develop hTRT-specific CTL, suggesting the existence of precursor CTL for h TRT in the repertoire of normal Individuals and in cancer patients.
Journal ArticleDOI
Transmission of endoplasmic reticulum stress and pro-inflammation from tumor cells to myeloid cells.
Navin R. Mahadevan,Jeffrey J. Rodvold,Homero Sepulveda,Steven S. Rossi,Angela F. Drew,Maurizio Zanetti +5 more
TL;DR: It is suggested that transmissible ER stress is a mechanism through which tumor cells can control myeloid cells by directing them toward a proinflammatory phenotype, thus facilitating tumor progression.
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Evolutionary pressure against MHC class II binding cancer mutations
Rachel Marty Pyke,Wesley K. Thompson,Rany M. Salem,Joan Font-Burgada,Joan Font-Burgada,Maurizio Zanetti,Hannah Carter +6 more
TL;DR: It is demonstrated that the M HC-II genotype constrains the mutational landscape during tumorigenesis in a manner complementary to MHC-I, emphasizing the central role of MHC -II presentation in tumor evolution.
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Tapping CD4 T cells for cancer immunotherapy: the choice of personalized genomics.
TL;DR: The role and regulation of CD4 T cells in response to tumor Ags is discussed, and emphasis is placed on the types of Ags and mechanisms that elicit tumor-protective responses.
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Cell-Extrinsic Effects of Tumor ER Stress Imprint Myeloid Dendritic Cells and Impair CD8+ T Cell Priming
Navin R. Mahadevan,Veronika Anufreichik,Jeffrey J. Rodvold,Kevin Chiu,Homero Sepulveda,Maurizio Zanetti +5 more
TL;DR: It is demonstrated that tumor-borne ER stress imprints ab initio BMDC to a phenotype that recapitulates several of the inflammatory/suppressive characteristics ascribed to tumor-infiltrating myeloid cells, highlighting the tumor UPR as a critical controller of anti-tumor immunity and a new target for immune modulation in cancer.