Objective Rheumatoid arthritis is genetically associated with the major histocompatibility complex class II region (HLA-DR4) suggesting involvement of T cell mediated autoimmune recognition of joint specific antigens. Only cartilage contain joint-specific proteins. The most widely used model is arthritis induced with type II collagen (CII), The major protein component of cartilage. To understand the role of CII-reactive T-cells a series of precisely designed transgenic mice are available in Lund. This includes mice with human CII instead of mouse CII in cartilage (obtained by crossing human CII transgenic with mouse CII deleted mice) and mice with functional expression of human DR4. They have already defined the epitope in human CII recognised by murine T cells. This epitope can be recognised in its glycosylated form. Partially tolerised T-cells against this epitope develop in mice expressing the epitope in cartilage and the mice will eventually develop arthritis. I will analyse the precise nature of the tolerance. The methods I will use include T-cell cloning, cytokine analysis and TCR sequencing. Fields of science medical and health sciencesclinical medicinerheumatologynatural sciencesbiological sciencesbiochemistrybiomoleculesproteins Programme(s) FP4-TMR - Specific research and technological development programme in the field of the training and mobility of researchers, 1994-1998 Topic(s) 0301 - Post-graduate research training grants TL02 - Molecular Biology and Biochemistry Call for proposal Data not available Funding Scheme RGI - Research grants (individual fellowships) Coordinator LUND UNIVERSITY EU contribution No data Address 39,Soelvegatan 19 , BMC:l11 221 84 LUND Sweden See on map Total cost No data Participants (1) Sort alphabetically Sort by EU Contribution Expand all Collapse all Not available France EU contribution No data Address See on map Total cost No data
