Abstract

Immunotherapies, such as chimeric antigen receptor (CAR) T-cells and immune checkpoint blockades (ICB), have transformed hematologic malignancy treatment options but have not had similar impacts on solid tumors (1, 2). These treatments are limited to finite target antigens or require a patient’s own primed antitumor T-cell population, respectively (3, 4). To overcome these limitations, we engineered conventional type 1 dendritic cells (DCs) with an antitumor binding, toll-like receptor 4 (TLR4) signaling CAR to harness the DCs ability to cross prime a broad repertoire of antitumor CD8 T-cells. In vitro, the CAR-DC lead to increased tumor uptake, DC maturation, and cross-priming of tumor-reactive CD8 T-cells. CAR-DCs lead to complete rejection of an orthotopic solid tumor model with heterogenous CAR target expression. The antitumor T-cell population from CAR-DC treated mice showed an improved T-cell response against more than one endogenous tumor antigen, increased activation, and more robust persistence of tumor-reactive clones.

Committee Chair

Carl DeSelm

Committee Members

Kenneth Murphy; Nathan Singh; Robert Schreiber; Todd Fehniger

Degree

Doctor of Philosophy (PhD)

Author's Department

Biology & Biomedical Sciences (Immunology)

Author's School

Graduate School of Arts and Sciences

Document Type

Dissertation

Date of Award

12-17-2025

Language

English (en)

Author's ORCID

0000-0001-5006-9020

Available for download on Thursday, December 16, 2027

Included in

Biology Commons

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