It is becoming clear that the CD137/CD137L interaction is unique and distinct from any other pathway with co-stimulatory properties (Figure 1.4). Given the effect of anti-CD137 mAb in protecting against disease, a major challenge is to streamline and design effective treatments for various autoimmune and non-autoimmune disorders. The fact that a novel regulatory CD11c+CD8+ cell population expanded by anti-CD137 mAb can block the development of autoimmune diseases provides an additional interest to CD137 signaling. Our laboratory, which was the first to describe this novel cell type, is actively pursuing the question whether these cells can replace anti-CD137 mAb therapy in combating various immune disorders. Our unpublished results thus far look promising and demonstrate that adoptively transferred CD11c+CD8+ (anti-CD137 mAb-expanded) cells are on par with anti-CD137 mAb therapy in treating inflammatory bowel disease and halting the spread of herpes simplex virus by selectively targeting autoreactive T cells.
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