Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

Host-dependent control of early regulatory and effector T-cell differentiation underlies the genetic susceptibility of RAG2-deficient mouse strains to transfer colitis

Valatas, V. ; He, J. ; Rivollier, Aymeric LU ; Kolios, G. ; Kitamura, K. and Kelsall, B. L. (2013) In Mucosal Immunology 6(3). p.601-611
Abstract
De novo differentiation of CD4(+) Foxp3(+) regulatory T cells (induced (i) Tregs) occurs preferentially in the gut-associated lymphoid tissues (GALT). We addressed the contribution of background genetic factors in affecting the balance of iTreg, T helper type 1 (Th1), and Th17 cell differentiation in GALT in vivo following the transfer of naive CD4(+) CD45RB(high) T cells to strains of RAG2-deficient mice with differential susceptibility to inflammatory colitis. iTregs represented up to 5% of CD4(+) T cells in mesenteric lymph nodes of less-susceptible C57BL/6RAG2(-/-) mice compared with <1% in highly susceptible C57BL/10RAG2(-/-) mice 2 weeks following T-cell transfer before the onset of colitis. Early Treg induction was correlated... (More)
De novo differentiation of CD4(+) Foxp3(+) regulatory T cells (induced (i) Tregs) occurs preferentially in the gut-associated lymphoid tissues (GALT). We addressed the contribution of background genetic factors in affecting the balance of iTreg, T helper type 1 (Th1), and Th17 cell differentiation in GALT in vivo following the transfer of naive CD4(+) CD45RB(high) T cells to strains of RAG2-deficient mice with differential susceptibility to inflammatory colitis. iTregs represented up to 5% of CD4(+) T cells in mesenteric lymph nodes of less-susceptible C57BL/6RAG2(-/-) mice compared with <1% in highly susceptible C57BL/10RAG2(-/-) mice 2 weeks following T-cell transfer before the onset of colitis. Early Treg induction was correlated inversely with effector cell expansion and the severity of colitis development, was controlled primarily by host and not T-cell-dependent factors, and was strongly associated with interleukin-12 (IL-12)/23 production by host CD11c(+) CD103(+) dendritic cells. These data highlight the importance of genetic factors regulating IL-12/23 production in controlling the balance between iTreg differentiation and effector-pathogenic CD4(+) T-cell expansion in lymphopenic mice and indicate a direct role for iTregs in the regulation of colonic inflammation in vivo. (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
Mucosal Immunology
volume
6
issue
3
pages
601 - 611
publisher
Nature Publishing Group
external identifiers
  • wos:000317722800016
  • scopus:84876346865
  • pmid:23149660
ISSN
1933-0219
DOI
10.1038/mi.2012.102
language
English
LU publication?
yes
id
06bf5e6c-138e-4da2-bf08-2d0fcace1fb6 (old id 3739018)
date added to LUP
2016-04-01 11:06:57
date last changed
2022-03-27 22:28:39
@article{06bf5e6c-138e-4da2-bf08-2d0fcace1fb6,
  abstract     = {{De novo differentiation of CD4(+) Foxp3(+) regulatory T cells (induced (i) Tregs) occurs preferentially in the gut-associated lymphoid tissues (GALT). We addressed the contribution of background genetic factors in affecting the balance of iTreg, T helper type 1 (Th1), and Th17 cell differentiation in GALT in vivo following the transfer of naive CD4(+) CD45RB(high) T cells to strains of RAG2-deficient mice with differential susceptibility to inflammatory colitis. iTregs represented up to 5% of CD4(+) T cells in mesenteric lymph nodes of less-susceptible C57BL/6RAG2(-/-) mice compared with &lt;1% in highly susceptible C57BL/10RAG2(-/-) mice 2 weeks following T-cell transfer before the onset of colitis. Early Treg induction was correlated inversely with effector cell expansion and the severity of colitis development, was controlled primarily by host and not T-cell-dependent factors, and was strongly associated with interleukin-12 (IL-12)/23 production by host CD11c(+) CD103(+) dendritic cells. These data highlight the importance of genetic factors regulating IL-12/23 production in controlling the balance between iTreg differentiation and effector-pathogenic CD4(+) T-cell expansion in lymphopenic mice and indicate a direct role for iTregs in the regulation of colonic inflammation in vivo.}},
  author       = {{Valatas, V. and He, J. and Rivollier, Aymeric and Kolios, G. and Kitamura, K. and Kelsall, B. L.}},
  issn         = {{1933-0219}},
  language     = {{eng}},
  number       = {{3}},
  pages        = {{601--611}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Mucosal Immunology}},
  title        = {{Host-dependent control of early regulatory and effector T-cell differentiation underlies the genetic susceptibility of RAG2-deficient mouse strains to transfer colitis}},
  url          = {{http://dx.doi.org/10.1038/mi.2012.102}},
  doi          = {{10.1038/mi.2012.102}},
  volume       = {{6}},
  year         = {{2013}},
}