Marcin Pekalski

After completing an MSc 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 in the DIL at the University of Oxford where I am using my research experience in linking genetic and environmental determinants of autoimmunity with immune system function and developing 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 am co-author of the synbiotic trial at GPPAD and lead for microbiome studies at PTChA. In this way, I am applying my experience in prevention strategies 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

Principal Investigator of Polish Society of Autoimmune Diseases:http://ptcha.pl/en/

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

* A. Rubio García, A. Paterou, M. Lee, H. Slawinski, L.S. Wicker, J.A. Todd, and M.L. Pekalski. 2019. Peripheral tolerance to insulin is encoded by mimicry in the microbiome. bioRxiv