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Marcin Pekalski

MRes PhD

Principal Scientist

Immunology, host microbiota interactions, immunotherapy, immune genetics, immune repertoire, data scientist, metagenomics, immune aging

After completing an MRes in Molecular Biology at Jagiellonian University and doctoral studies in Immunology at the University of Newcastle, I moved to the University of Cambridge to take up a Senior Research Associate position.

I am currently based at the Department of Peadiatrics, Wellcome Centre for Human Genetics, University of Oxford where I investigate genetic and environmental determinants of autoimmunity, link them with immune system function and develop T1D immunotherapies. This has led to a number of insights into T cell biology and two mechanistic trials using IL-2 as an intervention. 

After discovering antimicrobial receptors on recent thymic emigrants in neonates and adults, I hypothesised peripheral Treg induction to commensal mimotopes as the regulatory mechanism, entangled with thymic Tregs, conferring tolerance to human epitopes. I am particularly interested in linking the causal role of microbial dysbiosis, an environmental trigger of T1D, with host genetics (HLA class II, INS, PTPN22 and IL-2 pathway) and the immune repertoire (TCRs) against commensal mimotopes, in the aetiology of T1D*.

I am currently designing mechanistic microbiome intervention studies and author of the SINT1A trial at GPPAD and lead for microbiome research at PTChA. In this way, I am applying my experience in prevention strategies including dietary interventions to eradicate diseases linked with microbiome pathologies, in particular T1D, generating insights into the biology of the host-microbial interaction.

Key words: host-microbial interaction, autoimmunity, immunology, T cells, RTEs, Tregs, synbiotic, immunotherapy, HLA class II, TCR, IL-2, holobiont, dysbiosis, mimotope, mimicry, dietary fiber;

Major disease focus: Type 1 Diabetes (T1D), Multiple Sclerosis (MS);

Scientific Board member of Polish Society of Autoimmune Diseases:

Citation - Google Scholar:

Current Project Lead:

Peripheral tolerance to insulin is encoded by mimicry in the microbiome


HLA-DQβ57, anti-insulin T cells and insulin mimicry in autoimmune diabetes

Recent publications

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