Tumours escape the immune system by mutating to decrease their immunogenicity. In this study, now in @NatureComms, we described that immune cells can adapt to IFNg-driven escape, enhancing their fitness and thereby counteracting tumour escape nature.com/articles/s41467-0…
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How lytic cell death drives autoantigen release and fuels inflammation? With @lynndustinlab we ask this using a common autoantigen, TRIM21. The autoantigen TRIM21 assembles proinflammatory immune complexes after lytic cell death | Science Immunology science.org/eprint/VEVN4EQK8…
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Really pleased to see this Opinion Review out. The peptide selectivity model: Interpreting NK cell KIR-HLA-I binding interactions and their associations to human diseases: Trends in Immunology cell.com/trends/immunology/f…
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Exhausted T cells impede immune response in cancer. Immune checkpoint inhibitors, especially CTLA-4 blockade, show promise in rejuvenating T cell function for cancer immunotherapy. Gracie Jennah Mead writes. oncobites.blog/2024/01/17/ce…
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Don't forget, our DPhil in Cancer Science Programme is now open for applications! For more information - or for details on how to apply - visit our website ⬇️ cancer.ox.ac.uk/study @OxfordMedSci @mplsoxford
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Our new work led by our fantastic PhD student Jose (@j__cabezas) showing dramatic reductions in TCR-T cell cross-reactivity without modifying the TCR. Part of this work relied on SPR-based @carterra_bio to measure 163 TCR/pMHC affinities within 24 hours at 37 degrees.
I am excited to share the results from my PhD project at the @Dushek lab and my first first-author manuscript! Generation of T cells with reduced off-target cross-reactivities by engineering co-signalling receptors. biorxiv.org/content/10.1101/… 🧵
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Wonderful study from @Dushek lab that is a real breakthrough. I think they've solved 1/2 the problem of TCR cross-reactivity. They can make the (in)famous A3A TCR (that resulted in lethal cardiac toxicity) completely safe! Go read it to understand how!
Generation of T cells with reduced off-target cross-reactivities by engineering co-signalling receptors biorxiv.org/cgi/content/shor… #biorxiv_immuno
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#LocationLocationLocation! 💥Our new Feature Review on the regional specialization of the immune response along #airways is out @TrendsImmuno! We discuss anatomical, functional & microbiota factors controlling #innate & #adaptive #immunity! @david_hoytema authors.elsevier.com/a/1jzXg…
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Thinking of doing a PhD? Why not apply to study at Oxford? The Kennedy Institute @KIROxford are holding their first open day. Join us for… 🧫 Lab tours 🙋‍♀️Meet our students 📝Taster lectures 🔬Technology talks Find out more and book your place! 👉 kennedy.ox.ac.uk/study-with-…
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We are looking for a PhD student to study the immune relationship between cancer and atherosclerosis. Get in touch if interested! kennedy.ox.ac.uk/study-with-… cancer.ox.ac.uk/study#dphil-…
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How can we extend responses to KRASG12C drugs? Out now in @NatureComms, combining Revolution Medicines’ RAS(ON) G12C-selective inhibitor with a SHP2 inhibitor and immune checkpoint blockade to study their effects on KRAS-mutant lung tumours of varying immunogenicities.
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PhD/DPhil applications at the @KirOxford are now open for 2025! Check out all the projects; and then apply to our project 😀! Advertised with @AGerardLab to study macrophage signalling in tumours.
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Many cytosolic proteins are released by cell death. Why do some become autoantigens? In a team work led by Esther Jones and @LD53073604, we explore the story of a common autoantigen, TRIM21
Autoantigen TRIM21 (Ro52) assembles pro-inflammatory immune complexes following lytic cell death biorxiv.org/cgi/content/shor… #biorxiv_immuno
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