Sjögren syndrome and MIG

In the ductal epithelium adjacent to lymphoid infiltrates and in lymphocytes of salivary glands in patients with Sjögren syndrome (SS), there is an increased expression of monokine induced by interferon (IFN)-γ(MIG) and chemokine (C-X-C motif) receptor 3 (CXCR)3, which therefore seems to participate in the SS pathogenesis. Cultured SS salivary epithelial cells treated with IFN-γ release high levels of IFN-γ-inducible protein 10 (IP-10) and MIG. MIG secreted by salivary epithelial cells (under IFN-γ influence), recruits Type-1 helper (Th1) lymphocytes that create an amplification feedback loop, and perpetuates the autoimmune process, through an enhanced IFN-γ induction, that in turn stimulates an additional MIG secretion from epithelial cells. The high levels of MIG in saliva and tears indicate an immune Th1 dependent response. An amelioration of autoimmune sialadenitis with MIG antagonists has been observed in experimental settings, suggesting a possible therapeutic approach to SS. More investigations are needed to assess whether MIG is a novel therapeutic target for SS in humans.