Published online 10 October 2005 doi:10.1084/jem.20040662
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 202, Number 8, 1051-1061
Essential role for CD103 in the T cellmediated regulation of experimental colitis
Oliver Annacker1,
Janine L. Coombes1,
Vivianne Malmstrom2,
Holm H. Uhlig1,
Tim Bourne3,
Bengt Johansson-Lindbom4,
William W. Agace4,
Christina M. Parker5, and
Fiona Powrie1
1 Sir William Dunn School of Pathology, University of Oxford, OX1 3RE, England, UK
2 Unit of Rheumatology, Department of Medicine, Karolinska Institutet, 171 76 Stockholm, Sweden
3 Celltech R&D Limited, Slough, SL1 3WE, England, UK
4 Immunology Section, Biomedical Center I-13, S-221 84, Lund, Sweden
5 Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115
CORRESPONDENCE Fiona Powrie: fiona.powrie{at}pathology.ox.ac.uk
The integrin CD103 is highly expressed at mucosal sites, but its role in mucosal immune regulation remains poorly understood. We have analyzed the functional role of CD103 in intestinal immune regulation using the T cell transfer model of colitis. Our results show no mandatory role for CD103 expression on T cells for either the development or CD4+CD25+ regulatory T (T reg) cellmediated control of colitis. However, wild-type CD4+CD25+ T cells were unable to prevent colitis in immune-deficient recipients lacking CD103, demonstrating a nonredundant functional role for CD103 on host cells in T reg cellmediated intestinal immune regulation. NonT cell expression of CD103 is restricted primarily to CD11chighMHC class IIhigh dendritic cells (DCs). This DC population is present at a high frequency in the gut-associated lymphoid tissue and appears to mediate a distinct functional role. Thus, CD103+ DCs, but not their CD103 counterparts, promoted expression of the gut-homing receptor CCR9 on T cells. Conversely, CD103 DCs promoted the differentiation of IFN-
producing T cells. Collectively, these data suggest that CD103+ and CD103 DCs represent functionally distinct subsets and that CD103 expression on DCs influences the balance between effector and regulatory T cell activity in the intestine.
Abbreviations used: CFSE, carboxyfluorescein diacetate succinimidyl ester; GALT, gut-associated lymphoid tissue; IBD, inflammatory bowel disease; LP, lamina propria; MLN, mesenteric LN.
C.M. Parker's present address is Harvard Medical School, Office of Research, Boston, MA 02459.

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