CD8A and diabetes mellitus: This may reflect the formation of an immune complex between S4B6 mAb and endogenous IL-2 [39] and the inability of JES6-1 mAb to completely prevent their immunostimulatory effects on memory-like CD8+ T cells in vivo and would explain the enhanced accumulation of Clone 4 cells in the LN of long term anti-IL-2 treated mice that did not develop diabetes (see Fig. 3B).