The role of β7 integrins in CD8 T cell trafficking during an antiviral immune response

The requirement of beta 7 integrins for lymphocyte migration was examined during an ongoing immune response in vivo. Transgenic mice (OT-I) expressing an ovalbumin-specific major histocompatibility complex class I-restricted T cell receptor for antigen were rendered deficient in expression of all beta 7 integrins or only the alpha E beta 7 integrin. To quantitate the relative use of beta 7 integrins in migration in vivo, equal numbers of CT-I and OT-I-beta 7(-/-) or OT-I-alpha E-/- lymph node (LN) cells were adoptively transferred to normal mice. Although OT-I-beta 7(-/-) LN cells migrated to mesenteric LN and peripheral LN as well as wild-type cells, beta 7 integrins were required for naive CD8 T cell and B cell migration to Peyer's patch. After infection with a recombinant virus (vesicular stomatitis virus) encoding ovalbumin, beta 7 integrins became critical for migration of activated CD8 T cells to the mesenteric LN and Peyer's patch. Naive CD8 T cells did not enter the lamina propria or the intestinal epithelium, and the majority of migration of activated CD8 T cells to the small and large intestinal mucosa, including the epithelium, was beta 7 integrin-mediated. The alpha E beta 7 integrin appeared to play no role in migration during a primary CD8 T cell immune response in vivo. Furthermore, despite dramatic upregulation of alpha E beta 7 by CD8 T cells after entry into the epithelium, long-term retention of intestinal intraepithelial lymphocytes was also alpha E beta 7 independent.