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RISS 인기검색어
- 검색키워드
- 저자 : Rutgeerts, P. (검색결과 1 건)
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Maerten, P.,Kwon, B. S.,Shen, C.,De Hertogh, G.,Cadot, P.,Bullens, D. M. A.,Overbergh, L.,Mathieu, C.,Van Assche, G.,Geboes, K.,Rutgeerts, P.,Ceuppens, J. L. Blackwell Science Ltd 2006 Clinical and experimental immunology Vol.143 No.2
<P>Summary</P><P>4-1BB ligand (4-1BBL) expressed on antigen-presenting cells interacts with 4-1BB on activated T cells (especially CD8<SUP>+</SUP> cells) and co-stimulates the latter to secrete cytokines and to proliferate. The role of 4-1BB−4-1BBL interaction was studied here in a model of colitis based on naive CD4<SUP>+</SUP> T cell transfer to SCID mice, a disease model in which CD8 cells do not take part. We found that CD4<SUP>+</SUP> T cells from 4-1BB-deficient mice, after transfer in SCID mice, proliferated more rapidly compared to wild-type CD4<SUP>+</SUP> T cells. Mice reconstituted with naive CD4<SUP>+</SUP> T cells from 4-1BB-deficient mice developed colitis, however, with a mixed Th1/Th2 response, in contrast to the Th1-type response in mice reconstituted with wild-type naive CD4<SUP>+</SUP> T cells. Importantly, this altered cytokine response did not temper colitis severity. Although it has been reported previously that 4-1BB co-stimulation may contribute to regulatory T cell functioning, we found that CD4<SUP>+</SUP>CD25<SUP>+</SUP> regulatory T cells from 4-1BB-deficient mice were perfectly able to prevent naive CD4<SUP>+</SUP> T cell-induced colitis. In conclusion, our data provide evidence that 4-1BB−4-1BBL interaction modulates the effector CD4<SUP>+</SUP> T cell-driven immune response and cytokine production in experimental colitis without affecting regulatory T cell function.</P>
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