Immunopathogenic and regulatory mechanisms in autoimmune diseases and chronic inflamation

Mediators produced by antigen-presenting and T cells are dominant in orchestrating both autoimmune and chronic inflammatory diseases. However, timing of their action, regulation of activation and overall contribution to tissue damage are still not completely known. This project aims to establish relation of gene variants, expression and cell distribution of TLRs, CD40, Th1/Th17 cytokines and other related molecules with initiation, course and therapy response in multiple sclerosis (MS), psoriasis and chronic graft rejection. This goal will be achieved experimentally with EAE as a model and in clinical setting using samples from affected patients. Results from EAE are expected to improve understanding of its pathogenesis and will be translated to MS study. In addition, clinical part of the project will address the role of examined molecules in therapy outcome in relation to genetics in MS, psoriasis and chronic kidney rejection. We will also test the potential value of these molecules as biomarkers in urine and blood samples and define frequency of allelic variants for their loci by genetic profiling. Therefore, our results may contribute to: clarification of immunopathogenesis, identification of new therapeutic targets and defining biomarkers for prognosis, monitoring and validation of treatment of chronic inflammation in MS, psoriasis and kidney transplantation. Possibly, genetic analysis will reveal some ethnic specificity of our patients.