$TCR{gamma}{delta}^+T$ cells play a critical role in protecting the intestinal mucosa against pathogenic infection. In the absence of infection, $TCR{gamma}{delta}^+T$T cell activation must be continuously regulated by T regulatory cells (Treg) to prevent the development of colitis. However, the activation of intestinal $TCR{gamma}{delta}^+T$ cells under normal conditions has not been clearly resolved. In order to determine $TCR{gamma}{delta}^+T$ cell activation in vivo, we designed an NF-${kappa}B$ based reporter system. Using the recombinant lentiviral method, we delivered the NF-${kappa}B$ reporter to isolated $TCR{gamma}{delta}^+T$T cells, which were then adoptively transferred into normal mice. Our data indicate that the NF-${kappa}B$ activation level in $TCR{gamma}{delta}^+T$T cells is higher in the intestinal intraepithelial layer than in the lamina propria region. In addition, the surface expression level of lymphocyte activation marker CD69 in $TCR{gamma}{delta}^+T$ cells is also higher in the intestinal intraepithelial layer and this activation was reduced by Sulfatrim treatment which removes of commensal bacteria. Collectively, our data indicate that the $TCR{gamma}{delta}^+T$ cell population attached to the intestinal lumen is constitutively activated even by normal commensal bacteria.