The Mitf gene is known to be expressed in melanocytes and we have shown that MITF is expressed in a subset of CNS neurons. A microarray expression study showed that many genes associated with the immune system and especially innate immunity were upregulated in the  Mitf mutant mouse CNS, compared to  the heterozygote.  Histological analysis of mutant mice did not show any clear sign of inflammation. To determine whether inflammation could be detected at the protein level, CNS samples were stained for  GFAP and Iba-1. Results, based on signal area, suggest an increase in astrogliosis and activation of microglia. Subsequently,  expression of selected genes involved in inflammation was determined. This showed changes in the expression of iba-1 and a possible increase in expression of CD11. Together, this suggests that the Mitf  mutant mice and heterozygotes have low level inflammation in the CNS and  possibly increased susceptibility to infection.  Mitf mutant mice have a reduced number of mast cells  (e.g. absent in the peritoneal cavity).  As mast cells are present in the brain meninges and are known to orchestrate the immune response in this tissue, the number of mast cells in the cortical meninges was determined. This analysis showed an absence of differentiated mast cells in the Mitf mutant mice but no significant decrease  in heterozygotes. While it is difficult to rule out other factors, it is likely that this lack of meningeal mast cells explains the apparent low level neuroinflammation in the mutant mouse but the phenotype of the heterozygote mice can not be explained by the lack of mast cells. A possibility is that a single copy of Mitf is not sufficient for fully functional mast cells.  The Mitf mutant mouse  could be a useful model for the role of mast cells in neuroinflammation and meningitis.