Computational immunologist focusing on #HLA in #infectious, #autoimmune diseases and #cancer. #immunology #immune #tumor #MHC #bioinformatics #immunotherapy

Szeged, Hungary
Joined December 2013
I C U mutant! Our new paper is out! Our immune system doesn’t just fight viruses – it edits them. APOBEC enzymes introduce C>U mutations that often make viral proteins easier for HLA molecules and T-cells to detect, boosting immune recognition. nature.com/articles/s41467-0… #COVID_19
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1/3 🧬 Our review is out in @NatureRevMicro! How can we develop #antibiotics that remain effective as bacteria evolve? Our answer: make #resistance evolution part of drug development from the very beginning.
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Mate Manczinger retweeted
📢 Paper Alert! Grateful to have been involved in this amazing work by @research_lazar and SzilviaJuhasz labs, presenting a framework for dissecting pathogen-host-drug interactions. #Pathogen #Virulence #SingleCell #DeepLearning @SysbioS Check it at: shorturl.at/LQUFP 👇
Counting bacteria is not enough. To understand what makes a bacterium dangerous, we need to see what it actually does when it meets human cells. Our MALVINA study is now out in @NatureComms
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Moreover, HLA variants with broader peptide-binding specificity are also associated with stronger antibody responses following influenza vaccination. Check out our article to learn more!
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It was a wonderful collaboration with Thomas Vogl at Medical University of Vienna and @SashaZhernakova at @univgroningen I am also grateful to my research group @BiologicalRese1 immunoinfo.hu
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Mate Manczinger retweeted
Can harmful gene loss become an evolutionary opportunity? In our new work in @OfficialSMBE, lab-evolved E. coli lines recovering from metabolic gene loss did more than return to normal: some surpassed wild-type on nutrients never seen during lab evolution. doi.org/10.1093/molbev/msag1…
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Mate Manczinger retweeted
Big progress vs cancer, folks. The kind of event curves from randomized trials that we've not seen before for a couple of the most deadly cancers. Congrats to the oncology research community for getting these trial done. #ASCO26, @ASCO
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8/ But there’s nuance inside AAS4: Among AAS4-driven tumors, specific HLA variants are enriched in immune-hot cases. So antigen presentation genetics may modulate whether an AAS4 tumor ends up “cold” vs “hot.”
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9/ Takeaway: Protein-level mutation patterns provide a complementary lens to DNA mutational signatures—linking mutagenesis + repair defects to peptide properties, immune contexture, and therapy response.
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