Host-dependent control of early regulatory and effector T-cell differentiation underlies the genetic susceptibility of RAG2-deficient mouse strains to transfer colitis
(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:
https://lup.lub.lu.se/record/3739018
- author
- Valatas, V. ; He, J. ; Rivollier, Aymeric LU ; Kolios, G. ; Kitamura, K. and Kelsall, B. L.
- organization
- publishing date
- 2013
- 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 <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}}, }