Abstract

TCRγδ+ T cells play a critical role in protecting the intestinal mucosa against pathogenic infection. In the absence of infection, TCRγδ+ T cell activation must be continuously regulated by T regulatory cells (Treg) to prevent the development of colitis. However, the activation of intestinal TCRγδ+ T cells under normal conditions has not been clearly resolved. In order to determine TCRγδ+ T cell activation in vivo, we designed an NF-κB based reporter system. Using the recombinant lentiviral method, we delivered the NF-κB reporter to isolated TCRγδ+ T cells, which were then adoptively transferred into normal mice. Our data indicate that the NF-κB activation level in TCRγδ+ 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 TCRγδ+ 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 TCRγδ+ T cell population attached to the intestinal lumen is constitutively activated even by normal commensal bacteria.

• Keywords: TCRγδ+ T cell; intestine; NF-κB; commensal bacteria