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Differential homing mechanisms regulate regionalized effector CD8 alpha beta(+) T cell accumulation within the small intestine

In English

Författare

Summary, in English

The CC chemokine receptor (CCR)9 is expressed on the majority of small intestinal, but few colonic, T cells, whereas its ligand CCL25 is constitutively expressed by small intestinal epithelial cells. As such, CCR9/CCL25 have been proposed to play a central role in regulating small intestinal but not colonic immune responses and thus to organize regionalized immunity within the intestinal mucosa. Here, we demonstrate that CCL25 is expressed at reduced levels by epithelial cells in the distal compared with proximal small intestine, which correlated with less efficient CCR9-dependent effector CD8 alpha ss(+) T cell entry into the ileal epithelium. In vitro-generated alpha(4)ss(+)(7) effector CD8 alpha ss(+) T cell entry into the lamina propria was less dependent on CCR9 than entry into the epithelium along the entire length of the small intestine and in particular in the ileum. CCR9-independent alpha(4)ss(+)(7) effector CD8 alpha ss(+) T cell entry was pertussis toxin-sensitive, suggesting a role for additional Gal-linked G protein-coupled receptors. Finally, in vivo-primed effector CD8 alpha ss(+) T cells displayed regionalized differences in their entry to the small intestinal epithelium with enhanced CCR9-independent entry to the ileum. These results highlight a hitherto underappreciated compartmentalization of immune responses within the small intestine and have direct implications for targeting strategies aimed at regulating T cell localization to the small intestinal mucosa.

Avdelning/ar

  • Immunology

Publiceringsår

2007

Språk

Engelska

Sidor

10122-10127

Publikation/Tidskrift/Serie

Proceedings of the National Academy of Sciences

Volym

104

Issue

24

Dokumenttyp

Artikel i tidskrift

Förlag

National Academy of Sciences

Ämne

  • Immunology in the medical area

Nyckelord

  • chemokine receptor
  • intestinal mucosa

Status

Published

Forskningsgrupp

  • Immunology

ISBN/ISSN/Övrigt

  • ISSN: 1091-6490