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CUTTING EDGE |
*
Department of Tumor Progression and Immune Defense, German Cancer Research Center, Heidelberg, Germany; and
Basel Institute for Immunology, Basel, Switzerland
Inflammatory bowel disease is a quite severe chronic
inflammation, treated mainly by immunosuppression, which often has
serious side effects. As CD44 is important in lymphocyte activation and
migration, we asked whether Abs against CD44 isoforms influence
trinitrobenzenesulfonic acid (TNBS)-induced colitis in mice. A lethal
colitis (73/111 mice) could be prevented in 69 of 97 mice by
anti-CD44v7 (CD44 variant isoform v7), whereas anti-CD44s (CD44
standard isoform) and anti-CD44v6 had no effect. Upon receiving
anti-CD44v7 after the disease had been fully exacerbated, >90% of
the mice recovered. TNBS plus anti-CD44v7-treated mice developed
early signs of inflammation, with infiltration of leukocytes in the
lamina propria and increased IFN-
production. However, while control
mice developed a severe pancolitis, the intestine fully regenerated in
anti-CD44v7-treated mice. Locally and systemically, a strong
increase in IL-10 production was noted. Thus, anti-CD44v7 can be
regarded as a highly efficient and specific therapeutic reagent in
chronic colitis, which probably functions by regulating an overshooting
Th1 reaction.
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