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Title: Involvement of 4-1BB (CD137)-4-1BBligand interaction in the modulation of CD4 T cell-mediated inflammatory colitis
Authors: Maerten, Philippe ×
Kwon, BS
Shen, Chong
De Hertogh, Gert
Cadot, Pascal
Bullens, Dominique
Overbergh, Lutgart
Mathieu, Chantal
Van Assche, Gert
Geboes, Karel
Rutgeerts, Paul
Ceuppens, Jan #
Issue Date: Feb-2006
Publisher: Blackwell Science Ltd.
Series Title: Clinical and Experimental Immunology vol:143 issue:2 pages:228-236
Abstract: 4-1BB ligand (4-1BBL) expressed on antigen-presenting cells interacts with 4-1BB on activated T cells (especially CD8+ 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+ T cell transfer to SCID mice, a disease model in which CD8 cells do not take part. We found that CD4+ T cells from 4-1BB-deficient mice, after transfer in SCID mice, proliferated more rapidly compared to wild-type CD4+ T cells. Mice reconstituted with naive CD4+ 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+ 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+CD25+ regulatory T cells from 4-1BB-deficient mice were perfectly able to prevent naive CD4+ T cell-induced colitis. In conclusion, our data provide evidence that 4-1BB-4-1BBL interaction modulates the effector CD4+ T cell-driven immune response and cytokine production in experimental colitis without affecting regulatory T cell function.
ISSN: 0009-9104
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Translational Cell & Tissue Research
Laboratory of Clinical Immunology
Clinical and Experimental Endocrinology
Translational Research in GastroIntestinal Disorders
Laboratory of Pediatric Immunology
× corresponding author
# (joint) last author

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