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Josef W. Goldufsky

Researcher at Rush University Medical Center

Publications -  17
Citations -  442

Josef W. Goldufsky is an academic researcher from Rush University Medical Center. The author has contributed to research in topics: Immunotherapy & Effector. The author has an hindex of 10, co-authored 12 publications receiving 243 citations.

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Intratumoral injection of the seasonal flu shot converts immunologically cold tumors to hot and serves as an immunotherapy for cancer

TL;DR: It is reported that unadjuvanted seasonal influenza vaccination via intratumoral, but not intramuscular, injection converts “cold” tumors to hot, generates systemic CD8+ T cell-mediated antitumor immunity, and sensitizes resistant tumors to checkpoint blockade, and proposes that antipathogen vaccines may be utilized for both infection prevention and repurposing as a cancer immunotherapy.
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Pseudomonas aeruginosa ExoT Induces Mitochondrial Apoptosis in Target Host Cells in a Manner That Depends on Its GTPase-activating Protein (GAP) Domain Activity.

TL;DR: It is demonstrated that the GAP domain activity is both necessary and sufficient to induce mitochondrial (intrinsic) apoptosis and is completely dependent on caspase-9 activity.
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Pseudomonas aeruginosa uses T3SS to inhibit diabetic wound healing.

TL;DR: Data demonstrate that P. aeruginosa establishes a robust and persistent infection in diabetic wounds independent of its ability to form biofilm and causes severe wound damage in a manner that primarily depends on its T3SS.
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Apoptosis and Compensatory Proliferation Signaling Are Coupled by CrkI-Containing Microvesicles

TL;DR: It is demonstrated that a fraction of apoptotic cells produce and release CrkI-containing microvesicles, which induce proliferation in neighboring cells upon contact, and that c-Jun amino-terminal kinase (JNK) plays a pivotal role in mediating vesicle-induced CPS in recipient cells.
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IL-15 Complexes Induce Migration of Resting Memory CD8 T Cells into Mucosal Tissues

TL;DR: It is demonstrated that IL-15 influences the generation of memory CD8 T cells by first promoting their accumulation into mucosal tissues and second by sustaining expression of Bcl-6 and T-bet, which is largely dependent on mammalian target of rapamycin and its subsequent inactivation of FoxO1.