P
Pamela M. Odorizzi
Researcher at University of Pennsylvania
Publications - 30
Citations - 6077
Pamela M. Odorizzi is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Immune system & Cytotoxic T cell. The author has an hindex of 18, co-authored 26 publications receiving 4761 citations. Previous affiliations of Pamela M. Odorizzi include University of California, San Francisco.
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Journal ArticleDOI
Radiation and dual checkpoint blockade activate non-redundant immune mechanisms in cancer
Christina Twyman-Saint Victor,Andrew J. Rech,Amit Maity,Ramesh Rengan,Ramesh Rengan,Kristen E. Pauken,Erietta Stelekati,Joseph L. Benci,Bihui Xu,Hannah Dada,Pamela M. Odorizzi,Ramin S. Herati,Kathleen D. Mansfield,Dana Patsch,Ravi K. Amaravadi,Lynn M. Schuchter,Hemant Ishwaran,Rosemarie Mick,Daniel A. Pryma,Xiaowei Xu,Michael Feldman,Tara C. Gangadhar,Stephen M. Hahn,E. John Wherry,Robert H. Vonderheide,Andy J. Minn +25 more
TL;DR: Major tumour regressions are reported in a subset of patients with metastatic melanoma treated with an anti-CTLA4 antibody and radiation and reproduced this effect in mouse models, showing that PD-L1 on melanoma cells allows tumours to escape anti- NCTLA4-based therapy, and the combination of radiation, anti- CTLA4 and anti-PD-L 1 promotes response and immunity through distinct mechanisms.
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Epigenetic stability of exhausted T cells limits durability of reinvigoration by PD-1 blockade
Kristen E. Pauken,Morgan A. Sammons,Pamela M. Odorizzi,Sasikanth Manne,Jernej Godec,Omar Khan,Adam M. Drake,Zeyu Chen,Debattama R. Sen,Makoto Kurachi,R. Anthony Barnitz,Caroline Bartman,Bertram Bengsch,Alexander C. Huang,Jason M. Schenkel,Golnaz Vahedi,W. Nicholas Haining,W. Nicholas Haining,Shelley L. Berger,E. John Wherry +19 more
TL;DR: The data indicate that epigenetic fate inflexibility may limit current immunotherapies, and PD-1 pathway blockade resulted in transcriptional rewiring and reengagement of effector circuitry in the TEX epigenetic landscape.
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Progenitor and terminal subsets of CD8+ T cells cooperate to contain chronic viral infection.
Michael A. Paley,Daniela C. Kroy,Pamela M. Odorizzi,Jonathan B. Johnnidis,Douglas V. Dolfi,Burton E. Barnett,Elizabeth K. Bikoff,Elizabeth J. Robertson,Georg M. Lauer,Steven L. Reiner,E. John Wherry +10 more
TL;DR: It is demonstrated that the T-box transcription factors T-bet and Eomesodermin differentially regulate two phenotypically and functionally distinct subsets of antiviral CD8+ T cells in mice, which may be important for antiviral immunity during chronic viral infections in humans.
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Bioenergetic Insufficiencies Due to Metabolic Alterations Regulated by the Inhibitory Receptor PD-1 Are an Early Driver of CD8+ T Cell Exhaustion
Bertram Bengsch,Andy L. Johnson,Makoto Kurachi,Pamela M. Odorizzi,Kristen E. Pauken,John Attanasio,Erietta Stelekati,Laura M. McLane,Michael A. Paley,Greg M. Delgoffe,E. John Wherry +10 more
TL;DR: A key metabolic control event early in exhaustion is highlighted and it is suggested that manipulating glycolytic and mitochondrial metabolism might enhance checkpoint blockade outcomes.
Journal ArticleDOI
Molecular and Transcriptional Basis of CD4+ T Cell Dysfunction during Chronic Infection
Alison Crawford,Jill M. Angelosanto,Charlly Kao,Travis A. Doering,Pamela M. Odorizzi,Burton E. Barnett,E. John Wherry +6 more
TL;DR: This study defined the phenotypic, functional, and molecular profiles of exhausted CD4(+) T cells and demonstrated unappreciated roles for transcription factors (TFs) including Helios, type I interferon (IFN-I) signaling, and a diverse set of coinhibitory and costimulatory molecules during CD4 (+) T cell exhaustion.