The intestinal mucosa contains unique sites designed for promoting specialized T cell responses. Oral infection with a murinized Listeria monocytogenes (Lm) induced a robust mucosal CD8 T cell response which rapidly converted to a memory population during the peak of the intestinal T cell response. Concomitant with this event, the mice were nearly completely protected against re-infection. Blocking migration with anti-α4β7 from 7 dpi prevented continued migration into the intestinal compartment but did not alter the rapid conversion of early migrating cells into memory suggesting in situ events regulated early memory formation. These early memory cells, but not other effector subsets, preferentially upregulated CD103 identifying them as precursors to mucosal resident memory CD8 T cells. Surprisingly, CD103 expression on infiltrating CD8 T cells was required for early T cell entry into the epithelium but not for long term retention. Moreover, CD103 upregulation on Lm-specific CD8 T cells within the epithelium was predominately independent of TGFβ signals. Thus, the generation of distinct CD8 T cell subsets uniquely tailored to respond to intestinal pathogens may be a hallmark of oral challenge. Indeed, CD8 T cells that infiltrate the intestinal mucosa following intranasal influenza virus infection failed to generate MPECs and were not maintained long-term, demonstrating the importance of intestinal priming for generating robust mucosal memory CD8 T cells.
- Copyright © 2013 by The American Association of Immunologists, Inc.