This project explores USP18’s role as a regulator of Type I interferon (IFN-I) signaling in immune cells, focusing on T cell activation and its potential relevance to immune-related diseases. My prior research shows that inhibiting USP18 enhances T cell responses, suggesting it as a therapeutic target. Using UK Biobank’s proteomic data, I aim to extend these findings to a population level.
Research Questions:
How does USP18 expression correlate with proteomic profiles of immune cells?
What downstream proteomic changes are linked to USP18 in IFN-I signaling pathways?
Can USP18-related proteomic signatures predict immune-related disease outcomes?
Objectives:
Analyze USP18 expression patterns across immune cell subsets in UK Biobank proteomic data.
Identify proteomic changes tied to USP18, focusing on pathways like JAK-STAT signaling and T cell activation markers (e.g., CD69, IL-8).
Correlate USP18 proteomic signatures with clinical data (e.g., cancer, viral infections) to assess disease associations.
Scientific Rationale:
My experimental work demonstrates that USP18 inhibition boosts T cell activation (e.g., increased CD69 and IL-8 expression), modulating IFN-I responses. These findings, while promising, are from small-scale studies. UK Biobank’s proteomic and clinical data offer a powerful resource to validate and broaden these insights, elucidating USP18’s role in immune regulation and its potential for clinical applications in immune-related diseases.