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Natural killer T cells (NK-T) immunoregulation by VIP: functional analysis, mechanisms of action and effects on type 1 diabetes as a model of Th1 type autoimmnune disease


The immune system and the brain continuously signal each other, often along the same pathways, which may explain the connection between immunity, mind and disease. Part of this communication network is represented by neuropeptides and their receptors and recent findings can now address the issue of relevance to health, proving a potentially profound clinical significance.

The vasoactive intestinal peptide (VIP) is a neuropeptide synthesized by immune cells that functionally has various characteristics to be considered as a possible therapeutic agent for Th1 driven diseases with inflammatory and autoimmune components. Immuno-mediated (type 1) diabetes is an incurable disease that is increasingly in incidence throughout the Western world. The discovery of Th1 and Th2 subsets has helped to explain the immunological basis for the diversity of T cell responses in autoimmune diseases such as type I diabetes. VIP is a potent anti-inflammatory agent, which regulates a broad spectrum of pro-inflammatory factors synthesized by both activated macrophages and microglia. Following antigenic stimulation, VIP is able to shift a Th1 immune response to a Th2 response.

The therapeutic effect of VIP on a model of rheumatoid arthritis and Crohn's disease, two inflammatory and Th1-mediated autoimmune diseases, demonstrates its efficacy to treat this kind of disorders. In this study, by using the principal and a well-established animal model (Non Obese Diabetic) for type I diabetes, we will asses the role of VIP as a candidate to modulate the onset of type I diabetes. Besides that, we will gather data about the cellular and molecular mechanisms involved in VIP-mediated immunomodulation on Natural Killer T (NK-T) cells and other regulatory T cells. The results are interesting to test th e endogenous immunomodulatory potential of VIP on suppressor mechanisms such as those exerted by NK-T cells.

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