Title Information
Title
Phosphoproteomic Analysis of T Cell Receptor and Chimeric Antigen Receptor Signalling: Pathway Discovery and Regulatory Mechanisms
Type of Resource (primo)
dissertations
Name: Personal
Name Part
Callahan, Aurora
Role
Role Term: Text
creator
Name: Personal
Name Part
Salomon, Arthur
Role
Role Term: Text
Advisor
Name: Personal
Name Part
Fawzi, Nicolas
Role
Role Term: Text
Reader
Name: Personal
Name Part
DeLong, Alison
Role
Role Term: Text
Reader
Name: Personal
Name Part
Beura, Lalit
Role
Role Term: Text
Reader
Name: Personal
Name Part
High, Anthony
Role
Role Term: Text
Reader
Name: Corporate
Name Part
Brown University. Department of Molecular Biology, Cell Biology and Biochemistry
Role
Role Term: Text
sponsor
Origin Information
Copyright Date
2026
Physical Description
Extent
lv, 408 p.
digitalOrigin
born digital
Note: thesis
Thesis (Ph. D.)--Brown University, 2026
Genre (aat)
theses
Abstract
Mass spectrometry (MS) based proteomics has revolutionised biological discovery by allowing for high-throughput, accurate quantification of proteins, posttranslational modifications, and protein-protein interactions. Proteomics has been instrumental in the discovery and characterisation of T cell biology, particularly in phosphorylation-based T cell receptor (TCR) and chimeric antigen receptor (CAR) signalling. Although we understand a great deal about TCR and CAR signalling in T cells, open questions remain regarding the precise regulatory mechanisms involved in activating and deactivating T cells, and whether T cells elicit responses from their target cells. There are three main aims of this work: (1) to evaluate and optimise methodology for identifying tyrosine phosphorylation using MS, (2) to use MS to understand the regulatory networks involved in TCR signalling and activation, and (3) to use MS to determine how CAR design impacts both CAR T cell function and the targeted cells. I determined that suspension-trapping proteins provides optimal recovery of peptides for downstream phosphotyrosine (pY)-MS analysis, and that the BOOST method enhances identification of a subset of low abundance pY sites in primary murine T cells. I showed that three historically redundant protein tyrosine phosphatases uniquely impact global pY abundance and signalling regulation, while two critical protein tyrosine kinases uniquely regulate mRNA regulatory proteins and differentially impact T cell activation. Finally I determined that pY signalling from CARs is largely driven by inclusion of TCRζ, and a native ligand-based CAR can activate pY signalling and induce proliferation in target cells. Together, this work defines workflows for pY site identification using MS, uncovers novel regulation governing T cell pY homeostasis, and identifies potential shortcomings of CAR T cell therapies.
Subject (fast) (authorityURI="http://id.worldcat.org/fast", valueURI="http://id.worldcat.org/fast/00968006")
Topic
Immunology
Subject (fast) (authorityURI="http://id.worldcat.org/fast", valueURI="http://id.worldcat.org/fast/01011435")
Topic
Mass spectrometry
Subject (fast) (authorityURI="http://id.worldcat.org/fast", valueURI="http://id.worldcat.org/fast/00845386")
Topic
Cancer--Immunotherapy
Language
Language Term (ISO639-2B)
English
Record Information
Record Content Source (marcorg)
RPB
Record Creation Date (encoding="iso8601")
20260516