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SummaryDeficiency in cd T cells aggravates colitis in animal models suggesting that cd T cells have regulatory properties. Therefore, proliferation, suppression and cytokine secretion of human cd T cells were determined in vitro. Human peripheral cd T cells were isolated from the whole blood of healthy donors by magnetic antibody cell sorting technology. The proliferation after CD3/CD28 stimulation was measured by 3 [H]thymidine incorporation. Interferon-c (IFN-c), interleukin-2 (IL-2), transforming growth factor-b (TGF-b) and IL-10 concentrations were measured by enzymelinked immunosorbent assay; TGF-b messenger RNA was also measured by reverse transcription-polymerase chain reaction. The expression of latency associated peptide (LAP), a TGF-b complex component, intracellular cytokine content and T helper cell proliferation were measured by flow cytometry. Human cd T cells showed poor proliferation upon CD3/ CD28 stimulation and suppressed T helper cell growth stronger than CD4 + CD25 + T cells, although cd T cells were FOXP3 negative. They secreted little IL-2 but high concentrations of IFN-c, IL-10 and TGF-b. When looking at LAP expression the Vd1 subset was found to be the main TGF-b producer compared to Vd2 T cells. Taken together, peripheral cd T cells have in vitro a more potent regulatory potential than CD4 + CD25 + cells regarding T helper cell suppression. This is most likely the result of strong TGF-b secretion, particularly by the Vd1 subset.

Inflammatory bowel disease (IBD) research has been performed in human in vitro studies and in in vivo studies using appropriate animal models. Such animal models allow both the examination of inflammatory processes (both early and late events) as well as the evaluation of new therapeutic modalities. Since the first description of the immune complex colitis in rabbits in 1961, overall 63 models have been described, most of which within the last decade. These IBD animal models can be divided into 5 different categories: (1) antigen-induced colitis and colitis induced by microbials; (2) other inducible forms of colitis (chemical, immunological, and physical); (3) genetic colitis models (transgenic and knock-out models); (4) adoptive transfer models, and (5) spontaneous colitis models. In spite of the high overall number of models, none of them is the ‘perfect’ model and therefore numerous aspects need to be considered when choosing one model for a particular study. Importantly, most clinical aspects (e.g. extraintestinal manifestations or fistula) have recently been described in one or the other model allowing further studies with relevance for almost all aspects of IBD. So far, IBD animal models have taught us important lessons, e.g. the requirement of T-helper cells in most models, the need of a particular genetic background, and the role of the flora in the initiation of IBD. It is expected that our understanding of IBD will further increase in a number of additional areas using animal models, e.g. exploring the role of the innate immune system in IBD.