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Published online 8 November 2004 doi:10.1084/jem.20041789
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 200, Number 10, 1289-1297
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T Cell–specific Inactivation of the Interleukin 10 Gene in Mice Results in Enhanced T Cell Responses but Normal Innate Responses to Lipopolysaccharide or Skin Irritation

Axel Roers1, Lisa Siewe1, Elke Strittmatter1, Martina Deckert2, Dirk Schlüter3,4, Werner Stenzel2, Achim D. Gruber5, Thomas Krieg1, Klaus Rajewsky6, and Werner Müller7

1 Department of Dermatology, University of Cologne, 50931 Cologne, Germany
2 Department of Neuropathology, University of Cologne, 50931 Cologne, Germany
3 Institut für Medizinische Mikrobiologie, Otto-von-Guericke Universität Magdeburg, D-39120 Magdeburg, Germany
4 Department of Medical Microbiology and Hygiene, University Hospital Mannheim, University of Heidelberg, D-68167 Mannheim, Germany
5 Department of Pathology, School of Veterinary Medicine Hannover, D-30559 Hannover, Germany
6 Center for Blood Research, Harvard Medical School, Boston, MA 02115
7 Department of Experimental Immunology, German Research Center for Biotechnology, D-38124 Braunschweig, Germany

Address correspondence to Axel Roers, Dept. of Dermatology, University of Cologne, Josef Stelzmann Str. 9, 50931 Cologne, Germany. Phone: 49-221-478-3196; Fax: 49-221-478-5949; email: axel.roers{at}uni-koeln.de

Interleukin (IL)-10 is a regulator of inflammatory responses and is secreted by a variety of different cell types including T cells. T regulatory cells have been shown to suppress immune responses by IL-10–dependent, but also IL-10–independent, mechanisms. Herein, we address the role of T cell–derived IL-10 in mice with an inactivation of the IL-10 gene restricted to T cells generated by Cre/loxP-mediated targeting of the IL-10 gene. Splenocytes from this T cell–specific mutant secrete increased amounts of proinflammatory cytokines after activation in vitro compared with show enhanced contact hypersensitivity reactions, and succumb to severe immunopathology upon infection with Toxoplasma gondii. Despite intact IL-10 genes in other cell types, the dysregulation of T cell responses observed in the T cell–specific IL-10 mutant closely resembles the phenotype in complete IL-10 deficiency. However, in contrast to complete IL-10 deficiency, sensitivity to endotoxic shock and irritant responses of the skin are not enhanced in the T cell–specific IL-10 mutant. Our data highlight the importance of T cell–derived IL-10 in the regulation of T cell responses and demonstrate that endotoxic shock and the irritant response of the skin are controlled by IL-10 from other cell types.

Key Words: cytokines • gene targeting • inflammation • inflammatory bowel disease • allergic contact dermatitis

Abbreviations used in this paper: DNCB, 2,4-dinitrochlorobenzene; IBD, inflammatory bowel disease; MCP-1, monocyte chemoattractant protein 1.


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