Abstract

This dissertation investigates the myeloid cell circuits that enforce immunosuppression in the tumor microenvironment and limit responses to immune checkpoint blockade. Using genetically engineered mouse models, germ-free and microbiota manipulation approaches, and a humanized inhibitory receptor transgenic system, we identify two complementary axes through which myeloid cells restrain anti-tumor immunity — one systemic and microbiota-dependent, one local and extracellular matrix-dependent. In the first, we demonstrate that TREM2 functions as a systemic brake on gut-tumor immune crosstalk: TREM2 deficiency combined with anti-PD-1 treatment reprograms intestinal macrophages, expands the commensal bacterium Ruminococcus gnavus, and drives migration of gut-imprinted TNF-producing CD4⁺ T cells to the tumor bed in a microbiota-dependent manner. In the second, we show that fibronectin deposited within the metastatic niche engages LILRB4 on tumor-infiltrating myeloid cells, locking them in a suppressive state through attenuation of JAK–STAT1 signaling, and that therapeutic blockade of this interaction reprograms the myeloid compartment toward an ISG-high, type I interferon-dependent anti-tumor state. Together, these findings define spatially distinct myeloid checkpoints operating at the systemic and local levels, identify R. gnavus as a candidate probiotic adjuvant for immunotherapy, and establish the Fn–LILRB4–IFNAR axis as a stromal immune checkpoint with direct therapeutic implications for fibronectin-rich solid tumors.

Committee Chair

Marco Colonna

Committee Members

David DeNardo; Gregory Longmore; Gwendalyn Randolph; Robert Schreiber

Degree

Doctor of Philosophy (PhD)

Author's Department

Biology & Biomedical Sciences (Cancer Biology)

Author's School

Graduate School of Arts and Sciences

Document Type

Dissertation

Date of Award

4-28-2026

Language

English (en)

Author's ORCID

https://orcid.org/0000-0002-2579-5140

Available for download on Thursday, April 27, 2028

Included in

Biology Commons

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