Expression data from regulatory T cells of lymph nodes from NOD and NOD.Drak2-/- mice

Drak2-deficient (Drak2-/-) mice are resistant to autoimmune disease, yet maintain the ability to effectively eliminate pathogens and tumors. Thus, DRAK2 is an ideal target to treat autoimmune disease. However, the mechanisms by which DRAK2 regulates autoimmune disease development, particularly in type 1 diabetes (T1D), remain unresolved. We demonstrate that the resistance to T1D in non-obese diabetic (NOD) mice was due to the absence of Drak2 in T cells and required the presence of regulatory T cells (Tregs). Regulatory T cells (CD4+ CD8- CD25+ CD45RBlo) sorted from lymph nodes of NOD and NOD.Drak2-/- mice were sorted for RNA extraction and microarray analysis.