|M.Sc Student||Nehoray Shachar|
|Subject||The Involvement of SRBI in Differentiation of Tr1 Cells|
in DDM1 Model
|Department||Department of Medicine||Supervisor||Professor Nathan Karin|
The pathogenesis of effector lineages of CD4 T cells that promote the development and progression of various inflammatory autoimmune diseases, including type I diabetes mellitus (T1DM) is regulated by at least two major subsets of regulatory T cells: FOXP3 and FOXP3- T cells. The latter fall into two major subtypes: Those that predominantly secrete IL-10 (Tr1). These experiments were initiated using the type I diabetes (T1DM) model in NOD mice. As for Tr1 cells, several approaches have been suggested to polarize and extend these cells. A major obstacle in studding the in vivo properties of polarized Tr1 cells is the lack of a biomarker that would assist following their fate and migratory properties.
We found that over activation about 10% of CD4 T cells express the cell transmembrane scavenger receptor B-I (SR-BI, in human Cla1), and that upon interacting with SR-BI specific autoantibodies, or a mAb that our lab developed with high specificity to SR-BI/Cla1, they become IL-10 producing Tregs. The current study focuses on exploring their role in T1DM, and in using our new mAb (E12 mAb) for intervention in the pathogenesis of this disease.