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Identifying IL-17 receptor functions in pancreatic beta cells

Identifying IL-17 receptor functions in pancreatic beta cells

PhD/Honours project

Type 1 diabetes (T1D) is a human disease involving progressive autoimmune destruction of the -cells in the pancreatic islets. Inflammatory cytokines and lymphocytes are important inducers of T1D, however their precise mechanisms of action in T1D pathogenesis remain unclear. A clearer understanding of these processes will provide better opportunities for therapeutic intervention in human T1D patients.

Recent advances in T1D research indicate that inflammatory type 17 immune responses are involved in the pathogenesis of T1D in NOD mice and humans, thus it is likely that type 17 immunity is a key pathogenic regulator of T1D. IL-17 family cytokines are powerful drivers of inflammation and there is increasing evidence that IL-17/IL-17 receptor signalling induces inflammatory pathways in pancreatic -cells and plays a pathogenic role in the development of T1D. This project aims to define novel type 17 associated pathogenic mechanisms in the context of T1D. Techniques will include use of gene deficient -cell lines and novel strains of knockout mice, islet isolation, immune cell transfer, histology, quantitative RT-PCR, ELISA, Western blotting and flow cytometry.

Supervised by:

  • Dr Andrew Sutherland
  • Prof Helen Thomas
  • Disease Focus:

  • Type 1 diabetes
  • Research Unit:

  • Islet biology