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Published online before print October 13, 2006

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(Journal of Leukocyte Biology. 2007;81:168-175.)
© 2007 by Society for Leukocyte Biology

Aggravation of intestinal inflammation by depletion/deficiency of T cells in different types of IBD animal models

Anja A. Kühl^*, Nina N. Pawlowski^*, Katja Grollich^*, Christoph Loddenkemper, Martin Zeitz^* and Jörg C. Hoffmann^*,1

^* Medizinische Klinik I, and
Institute of Pathology, Charité, University Medicine Berlin, Campus Benjamin Franklin, Berlin, Germany

¹Correspondence: Medizinische Klinik I Charité - Universitätsmedizin Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, Berlin D-12200, Germany. E-mail: joerg.hoffmann{at}charite.de

ABSTRACT

The role of T cells in inflammatory bowel disease (IBD) is still controversial. Although T cells induce IBD in immunodeficient animals, others suggest a protective role of T cells. Therefore, this study was conducted in order to elucidate the effect of T cell depletion/deficiency on different IBD animal models. Mice depleted of or deficient in T cells were exposed to dextran sodium sulfate (DSS) in order to induce colitis. In addition, T cells were depleted in mice with terminal ileitis (TNF^ARE) or colitis due to interleukin 2 deficiency (IL-2 ko). Finally, DSS-induced colitis was studied in mice deficient in interferon gamma (IFN- ko) upon T cell depletion. Depletion of T cells aggravated DSS-induced colitis and terminal ileitis of TNF^ARE mice. Exacerbated DSS-induced colitis was also found in T cell-deficient mice. IL-2 ko mice showed increased mortality upon early (starting at 4 wk of age) but not late depletion (starting at 8 wk of age). Early T cell depletion or deficiency resulted in increased IFN- production by both lamina propria lymphocytes and splenocytes in every model investigated herein. In IFN- ko mice, T cell depletion did not affect the development and course of DSS-induced colitis. The protective effect of T cells in IBD was confirmed in various IBD animal models. Particularly, during the early phase of intestinal inflammation, T cells appear to be important. The mechanism seems to involve the control of IFN- production and epithelial regeneration.

Key Words: colitis • epithelial regeneration • interferon • terminal ileitis