To explore the cellular mechanism underlying the modulation on the Th1/Th2 immune responses, we focused on the changes of co-stimulating molecules CD80/CD86 expressed on the monocytes/macrophages, the professional antigen-presenting cells that play a key role in the onset of chronic inflammation and obesity-associated insulin resistance of T2D [6,37-40]. This evidence concerns the gene CD86 and obesity due to melanocortin 4 receptor deficiency.