IRF8 Transcription-Factor-Dependent Classical Dendritic Cells Are Essential for Intestinal T Cell Homeostasis
(2016) In Immunity 44(4). p.860-874- Abstract
The role of dendritic cells (DCs) in intestinal immune homeostasis remains incompletely defined. Here we show that mice lacking IRF8 transcription-factor-dependent DCs had reduced numbers of T cells in the small intestine (SI), but not large intestine (LI), including an almost complete absence of SI CD8αβ+ and CD4+CD8αα+ T cells; the latter requiring β8 integrin expression by migratory IRF8 dependent CD103+CD11b- DCs. SI homing receptor induction was impaired during T cell priming in mesenteric lymph nodes (MLN), which correlated with a reduction in aldehyde dehydrogenase activity by SI-derived MLN DCs, and inefficient T cell localization to the SI. These mice also lacked intestinal... (More)
The role of dendritic cells (DCs) in intestinal immune homeostasis remains incompletely defined. Here we show that mice lacking IRF8 transcription-factor-dependent DCs had reduced numbers of T cells in the small intestine (SI), but not large intestine (LI), including an almost complete absence of SI CD8αβ+ and CD4+CD8αα+ T cells; the latter requiring β8 integrin expression by migratory IRF8 dependent CD103+CD11b- DCs. SI homing receptor induction was impaired during T cell priming in mesenteric lymph nodes (MLN), which correlated with a reduction in aldehyde dehydrogenase activity by SI-derived MLN DCs, and inefficient T cell localization to the SI. These mice also lacked intestinal T helper 1 (Th1) cells, and failed to support Th1 cell differentiation in MLN and mount Th1 cell responses to Trichuris muris infection. Collectively these results highlight multiple non-redundant roles for IRF8 dependent DCs in the maintenance of intestinal T cell homeostasis.
(Less)
- author
- organization
- publishing date
- 2016-04-19
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Immunity
- volume
- 44
- issue
- 4
- pages
- 15 pages
- publisher
- Cell Press
- external identifiers
-
- scopus:84962173629
- pmid:27067057
- wos:000374444300017
- ISSN
- 1074-7613
- DOI
- 10.1016/j.immuni.2016.02.008
- language
- English
- LU publication?
- yes
- id
- db00b0a5-ed63-4618-a677-6eba162bd14e
- date added to LUP
- 2016-05-31 12:43:19
- date last changed
- 2025-02-08 09:27:06
@article{db00b0a5-ed63-4618-a677-6eba162bd14e, abstract = {{<p>The role of dendritic cells (DCs) in intestinal immune homeostasis remains incompletely defined. Here we show that mice lacking IRF8 transcription-factor-dependent DCs had reduced numbers of T cells in the small intestine (SI), but not large intestine (LI), including an almost complete absence of SI CD8αβ<sup>+</sup> and CD4<sup>+</sup>CD8αα<sup>+</sup> T cells; the latter requiring β8 integrin expression by migratory IRF8 dependent CD103<sup>+</sup>CD11b<sup>-</sup> DCs. SI homing receptor induction was impaired during T cell priming in mesenteric lymph nodes (MLN), which correlated with a reduction in aldehyde dehydrogenase activity by SI-derived MLN DCs, and inefficient T cell localization to the SI. These mice also lacked intestinal T helper 1 (Th1) cells, and failed to support Th1 cell differentiation in MLN and mount Th1 cell responses to Trichuris muris infection. Collectively these results highlight multiple non-redundant roles for IRF8 dependent DCs in the maintenance of intestinal T cell homeostasis.</p>}}, author = {{Luda, Katarzyna M. and Joeris, Thorsten and Persson, Emma K. and Rivollier, Aymeric and Demiri, Mimoza and Sitnik, Katarzyna M. and Pool, Lieneke and Holm, Jacob B. and Melo-Gonzalez, Felipe and Richter, Lisa and Lambrecht, Bart N. and Kristiansen, Karsten and Travis, Mark A. and Svensson-Frej, Marcus and Kotarsky, Knut and Agace, William W.}}, issn = {{1074-7613}}, language = {{eng}}, month = {{04}}, number = {{4}}, pages = {{860--874}}, publisher = {{Cell Press}}, series = {{Immunity}}, title = {{IRF8 Transcription-Factor-Dependent Classical Dendritic Cells Are Essential for Intestinal T Cell Homeostasis}}, url = {{http://dx.doi.org/10.1016/j.immuni.2016.02.008}}, doi = {{10.1016/j.immuni.2016.02.008}}, volume = {{44}}, year = {{2016}}, }