Previous studies showed that CTLA-4 could induce T cell tolerance and attenuate T cell mediated immune responses by binding with co-stimulating molecules, B7-1 (CD80) and B7-2 (CD86) [6], and dysfunction of CTLA-4 was demonstrated to be implicated in various autoimmune diseases including type 1 diabetes mellitus (T1DM) [7,8]. Here, CD86 is linked to diabetes mellitus.