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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

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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Progenitor and terminal subsets of CD8+ T cells cooperate to contain chronic viral infection.

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

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.
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Molecular and Transcriptional Basis of CD4+ T Cell Dysfunction during Chronic Infection

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.