Dataset Information

Post-Translational Modification Analysis in TCR Complexes Using Mass Spectrometry

ABSTRACT: This study investigates the structural and biochemical characteristics of T cell receptors (TCRs) involved in immune recognition. Using mass spectrometry-based proteomics, we analyzed post-translational modifications (PTMs), including glycosylation patterns, of different TCR variants. These modifications provide insight into the molecular regulation of TCR function and their interaction with peptide-MHC complexes. Complementary biophysical analyses, such as mass photometry, were performed to understand the oligomeric states of TCR-pMHC complexes. The findings contribute to a deeper understanding of TCR regulation and immune signaling mechanisms.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): T Cell

DISEASE(S): Covid-19

SUBMITTER: CANER AKIL

LAB HEAD: DR CANER AKIL

PROVIDER: PXD066461 | Pride | 2025-08-07

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	Database.fasta	Fasta
	QEX01_MF_230414_CA-TCR01_062.raw	Raw
	QEX01_MF_230414_CA-TCR02_065.raw	Raw
	mzTab_Glycosylation.mzTab	Mztab

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Project description:Developmental checkpoints in stem/progenitor cells are critical to the determination, commitment and differentiation into distinct lineages. Cancer cells often retain expression of lineage-specific checkpoint proteins, but their potential impact in cancer remains elusive. T lymphocytes mature in the thymus following a highly orchestrated developmental process that entails the successive rearrangements and expression of T-cell receptor (TCR) genes. Low affinity recognition of self-peptide/MHC complexes (self-pMHC) presented by thymic epithelial cells by the TCR of CD4+CD8+ (DP) cortical thymocytes transduces positive selection signals that ultimately shape the developing T cell repertoire. DP thymocytes not receiving these signals die by lack of stimulation whereas those that recognize self-pMHC with high affinity undergo TCR-mediated apoptosis and negative selection. In T-cell acute lymphoblastic leukaemia (T-ALL), leukaemic transformation of maturating thymocytes results from the acquisition of multiple genetic and epigenetic alterations in oncogenes and tumour suppressor genes, that disrupt the normal regulatory circuits and drive clonal expansion of differentiation-arrested lymphoblasts. We show here that TCR triggering by negatively-selecting self-pMHC prevented T-ALL development and leukaemia maintenance in mice. Induction of TCR signalling by high affinity self-pMHC or treatment with monoclonal antibodies to the CD3 signalling chain (anti-CD3) caused massive leukaemic cell death and a gene expression program resembling that of thymocyte negative selection. Importantly, anti-CD3 treatment hampered leukaemogenesis in mice transplanted with either mouse or patient-derived T-ALLs. These data provide a rationale for targeted therapy based on anti-CD3 treatment of T-ALL patients and demonstrate that endogenous developmental checkpoint proteins are amenable to therapeutic intervention in cancer cells. Gene expression data from four culture conditions was performed for the following cells: ALL-SIL-TCRÎ±/Î²-GFP co-cultured on OP9-DL1 for 48 h, ALL-SIL-TCRÎ±/Î²-GFP without co-culture, ALL-SIL cells transduced with TLX shRNA (sh-TLX), and ALL-SIL transduced with sh-control vectors. All conditions are performed in two replicates.

Dataset Information

Post-Translational Modification Analysis in TCR Complexes Using Mass Spectrometry

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