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Reduced susceptibility to dextran sulphate sodium‐induced colitis in the interleukin‐2 heterozygous (IL‐2 +/– ) mouse
Author(s) -
Sund Malin,
Xu Li Li,
Rahman Arman,
Qian BiFeng,
Hammarström MarieLouise,
Danielsson Åke
Publication year - 2005
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2005.02123.x
Subject(s) - colitis , cd8 , cytokine , il 2 receptor , endocrinology , splenocyte , immunology , chemistry , medicine , interleukin , t cell , microbiology and biotechnology , biology , immune system
Summary Mice homozygous for an inactivation of the interleukin‐2 (IL‐2) gene develop a T‐cell dependent colitis. Heterozygous (IL‐2 +/– ) mice are clinically healthy but have been shown to express reduced levels of IL‐2 in the colon. Splenocytes from the IL‐2 +/– mice had a poorer proliferative response to polyclonal T‐cell activation and these mice have reduced numbers of intestinal regulatory T cells (CD4 + CD25 + cells) when compared to wild type mice. When exposed to dextran sulphate sodium (DSS) IL‐2 +/– mice showed a markedly reduced susceptibility to DSS‐induced colitis. While DSS treatment caused a marked increase in both CD4 + and CD8 + colonic T cells expressing increased levels of IL‐2, IL‐4, and IL‐10 in wild type mice none of these changes were seen in IL‐2 +/– mice. On the contrary, cytokine expression in intestinal T cells of IL‐2 +/– mice was actually reduced after DSS treatment. These results suggest that reduced levels of IL‐2 leads to attenuated activation and function of intestinal T cells in IL‐2 +/– mice and a failure to react adequately to DSS exposure.