Marcin Pekalski

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: http://ptcha.pl/en/

Citation - Google Scholar: https://scholar.google.com/citations?user=85gPSaAAAAAJ&hl=en

https://www.well.ox.ac.uk/news/new-avenue-in-microbial-defence-in-newborn-children

Current Project Lead:

Peripheral tolerance to insulin is encoded by mimicry in the microbiome

https://www.biorxiv.org/content/10.1101/2019.12.18.881433v1.full

and

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

https://www.medrxiv.org/content/10.1101/2022.05.11.22274678v1