The results herein revealed that the treatment of STZ-induced T1DM mice with sodium citrate buffer, insulin and adoptively transferred dBMCs significantly decreased the level of glutamic acid decarboxylase antigen protein (GAD) comparing to that in naive mice received sodium citrate buffer (13.33 ± 1.27 pg/mg, 41.33 ± 1.76 pg/mg and 60.10 ± 1.42 pg/mg, respectively versus 100.17 ± 16.65 pg/mg) (Fig. 5D). Here, GAD1 is linked to type 1 diabetes mellitus.