Vasoactive intestinal peptide regulates Th17 function in autoimmune inflammation

Abstract

An imbalance of pro-inflammatory and anti-inflammatory cytokines, autoreactive and inflammatory T helper 1 (Th1) cells, and regulatory T (Treg) cells results in the loss of immune tolerance and the subsequent appearance of inflammatory autoimmune diseases. On the other hand, hormones and neuropeptides are endogenous factors controlling the immune homeostasis that have been proposed as therapeutic agents in different autoimmune disorders. Among them, the vasoactive intestinal peptide (VIP) has been shown to downregulate the inflammatory response and to alter the Th1/Th2 balance in favor of anti-inflammatory Th2 immune responses. Recent studies have revealed a greater diversification of the T cell effector repertoire with the identification of Th17 cells. This subpopulation has been shown to be pathogenic in several autoimmune diseases previously attributed to the Th1 lineage. Arising new data and a critical revision of already published studies indicate that VIP is an immunomodulatory therapeutic agent targeting the Th17/Treg pathway.