Objective In the NOD mouse, a valuable model for human IDDM, the diabetes susceptibility is linked to MHC II genes, but the mechanism(s) of influence at the T cell level are not yet clear. Using the established BDC2.5 TCR transgenic mouse line and making appropriate crosses into the B6, NOD and B6.H-2g7 background, 4 lines of mice could be obtained with homo- and heterozygous expression of the NOD MEIC H-2g7 or B6 MHC H-2b in the NOD or B6 background, respectively. The aim of this study is to investigate the protection mechanism(s) of the non-NOD MHC II Ab molecule on insulitis and IDDM. At first, two mice lines carrying knock-out alleles should be generates to confirm the direct role of the Ab molecule and to eliminate the contribution of non-transgenic TCRs. Furthermore, the T cells from the different mouse lines and the expression of MHC of MHC molecules in splenic antigen presenting cells (APSs)will be compared. Finally, the ability for these APSs to stimulate T cell proliferation and especially the influence on the Th1/Th2 balance should be investigated. Fields of science medical and health sciencesclinical medicineendocrinologydiabetes Programme(s) FP4-TMR - Specific research and technological development programme in the field of the training and mobility of researchers, 1994-1998 Topic(s) 0302 - Post-doctoral research training grants TL07 - Immunology and Cancer Call for proposal Data not available Funding Scheme RGI - Research grants (individual fellowships) Coordinator CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE Address Rue laurent fries 1 67404 Illkirch graffenstaden France See on map EU contribution € 0,00 Participants (1) Sort alphabetically Sort by EU Contribution Expand all Collapse all Not available Germany EU contribution € 0,00 Address See on map
