Please use this identifier to cite or link to this item:
http://bura.brunel.ac.uk/handle/2438/6663
Title: | CD4+CD25+ TR cells suppress innate immune pathology through cytokine-dependent mechanisms |
Authors: | Maloy, KJ Salaun, L Cahill, R Dougan, G Saunders, NJ Powrie, F |
Keywords: | Regulatory T cells;Helicobacter;Immune tolerance;Mucosal immunity;IL-10 |
Issue Date: | 2003 |
Publisher: | Rockefeller University Press |
Citation: | Journal of Experimental Medicine, 197(1): 111-119, Jan 2003 |
Abstract: | CD4+CD25+ regulatory T (TR) cells can inhibit a variety of autoimmune and inflammatory diseases, but the precise mechanisms by which they suppress immune responses in vivo remain unresolved. Here, we have used Helicobacter hepaticus infection of T cell–reconstituted recombination-activating gene (RAG)−/− mice as a model to study the ability of CD4+CD25+ TR cells to inhibit bacterially triggered intestinal inflammation. H. hepaticus infection elicited both T cell-mediated and T cell–independent intestinal inflammation, both of which were inhibited by adoptively transferred CD4+CD25+ TR cells. T cell–independent pathology was accompanied by activation of the innate immune system that was also inhibited by CD4+CD25+ TR cells. Suppression of innate immune pathology was dependent on T cell–derived interleukin 10 and also on the production of transforming growth factor β. Thus, CD4+CD25+ TR cells do not only suppress adaptive T cell responses, but are also able to control pathology mediated by innate immune mechanisms. |
Description: | Copyright @ 2003 The Rockefeller University Press |
URI: | http://jem.highwire.org/content/197/1/111.abstract http://bura.brunel.ac.uk/handle/2438/6663 |
DOI: | http://dx.doi.org/10.1084/jem.20021345 |
ISSN: | 0022-1007 |
Appears in Collections: | Biological Sciences Publications Dept of Life Sciences Research Papers |
Files in This Item:
File | Description | Size | Format | |
---|---|---|---|---|
Fulltext.pdf | 140.89 kB | Adobe PDF | View/Open |
Items in BURA are protected by copyright, with all rights reserved, unless otherwise indicated.