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Decoding NK Cell Licensing Through Programmable Nanoscale Clustering and Spatial Mapping

Project description

Natural killer immunology and receptor engineering for MHC-unrestricted immunotherapies

Natural killer (NK) cells kill tumour and virus-infected cells without prior sensitisation, but their clinical use is limited by the unclear mechanisms underlying their durable functional competence or ‘licensing’. Supported by the Marie Skłodowska-Curie Actions programme, the NK_LIC2CLUSTER_SR1 project will explore whether nanoscale clustering of inhibitory receptors encodes NK cell licensing, enabling the engineering of MHC-independent NK cells. It will assess whether clustering of Ly49A recruits phosphatases such as SHP-1 and creates licensing signatures that predict NK competence across MHC haplotypes. This work aims to advance MHC-unrestricted immunotherapies using insights from NK immunology and receptor engineering.

Objective

Natural killer (NK) cells are innate lymphocytes that kill tumor and virus-infected cells without prior sensitization, but clinical translation is hampered by limited mechanistic insight into how NKs attain durable functional competence or “licensing”.

NK_LIC2CLUSTER_SR1 will determine whether nanoscale clustering geometry of inhibitory receptors encodes licensing — a mechanistic insight that could enable engineering NK cells with predictable, MHC-independent, potency.

We will test whether ligand-independent clustering of the inhibitory receptor Ly49A recruits ITIM-associated phosphatases (e.g. SHP-1) and induces a licensing-like state in vivo, and whether quantitative nanoscale features (e.g. cluster size, density) form reproducible “licensing signatures” that predict NK competence across MHC haplotypes.

AIM 1 (causation): CRISPR knock-in of a chemically inducible Ly49A fusion at the Ncr1 locus in primary murine NKs will allow rapid, reversible clustering with a dimeriser. Functional (IFN-γ, CD107a, cytotoxicity, persistence, homing, tumor clearance) and mechanistic (ITIM phosphorylation, SHP-1 recruitment) readouts will be assessed ex vivo and after adoptive transfer into MHC-defined hosts.

AIM 2 (prediction & translation): Super-resolution imaging (SLML) and single-molecule mapping will quantify Ly49A and phospho-SHP-1 architectures across haplotypes. Spatial metrics will be integrated with functional data to derive reproducible licensing signatures and build predictive functional models.

The fellowship provides structured training and open-science outputs to accelerate fellow independence and maximise research impact. Leveraging worldwide expertise from the host labs in NK immunology, synthetic receptor engineering, advanced imaging, and computational modelling, the project will establish receptor topology as a mechanistic code for NK licensing, define nanoscale “licensing signatures,” and enable translational MHC-unrestricted immunotherapies.

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HORIZON-TMA-MSCA-PF-GF - HORIZON TMA MSCA Postdoctoral Fellowships - Global Fellowships

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(opens in new window) HORIZON-MSCA-2025-PF

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Coordinator

UNIVERSIDADE NOVA DE LISBOA
Net EU contribution

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€ 395 841,00
Address
CAMPUS DE CAMPOLIDE
1099-085 Lisboa
Portugal

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Activity type
Higher or Secondary Education Establishments
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