Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

Essential role for CD103 in the T cell-mediated regulation of experimental colitis

Annacker, O ; Coombes, JL ; Malmstrom, V ; Uhlig, HH ; Bourne, T ; Johansson Lindbom, Bengt LU ; Agace, William LU ; Parker, CM and Powrie, F (2005) In Journal of Experimental Medicine 202(8). p.1051-1061
Abstract
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) cell-mediated 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 cell-mediated intestinal immune regulation. Non-T cell expression of CD103 is restricted primarily to CD11c(high) MHC class IIhigh... (More)
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) cell-mediated 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 cell-mediated intestinal immune regulation. Non-T cell expression of CD103 is restricted primarily to CD11c(high) MHC 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-gamma-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. (Less)
Please use this url to cite or link to this publication:
author
; ; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Experimental Medicine
volume
202
issue
8
pages
1051 - 1061
publisher
Rockefeller University Press
external identifiers
  • wos:000232929500006
  • pmid:16216886
  • scopus:26844468978
  • pmid:16216886
ISSN
1540-9538
DOI
10.1084/jem.20040662
language
English
LU publication?
yes
id
e2118d0a-0a80-4d38-a216-7dddd89a95dc (old id 216500)
date added to LUP
2016-04-01 15:32:54
date last changed
2022-04-22 08:14:40
@article{e2118d0a-0a80-4d38-a216-7dddd89a95dc,
  abstract     = {{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) cell-mediated 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 cell-mediated intestinal immune regulation. Non-T cell expression of CD103 is restricted primarily to CD11c(high) MHC 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-gamma-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.}},
  author       = {{Annacker, O and Coombes, JL and Malmstrom, V and Uhlig, HH and Bourne, T and Johansson Lindbom, Bengt and Agace, William and Parker, CM and Powrie, F}},
  issn         = {{1540-9538}},
  language     = {{eng}},
  number       = {{8}},
  pages        = {{1051--1061}},
  publisher    = {{Rockefeller University Press}},
  series       = {{Journal of Experimental Medicine}},
  title        = {{Essential role for CD103 in the T cell-mediated regulation of experimental colitis}},
  url          = {{http://dx.doi.org/10.1084/jem.20040662}},
  doi          = {{10.1084/jem.20040662}},
  volume       = {{202}},
  year         = {{2005}},
}