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*
Nuffield Department of Surgery, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom; and
Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom
Transfer of CD45RBhigh CD4+ T cells to
immune-deficient mice in the absence of regulatory T cells leads to a
Th1-mediated colitis. In this study, we show that intestinal
inflammation is characterized by a 15-fold increase in the number of
CD134L+ (OX40L+)-activated DC in the mesenteric
lymph nodes (MLNs) compared with BALB/c mice. This was important
functionally, as administration of an anti-CD134L mAb inhibited the
proliferation of T cells in the MLNs as well as their expression of the
gut-homing integrin 
4
7. Most importantly,
the anti-CD134L mAb completely blocked development of colitis.
Surprisingly, CD134L was found to be expressed by a proportion of
dendritic cells (DC) in the MLNs of unreconstituted SCID mice,
suggesting that CD134L can be induced on DC in the absence of T
cell-derived signals. These results indicate that some DC in the MLNs
of SCID mice express an activated phenotype and that CD134L expression
by these cells is involved in the development of colitis induced by T
cell transfer. Accumulation of CD134L+ DC was inhibited by
cotransfer of regulatory T cells, suggesting that inhibition of the
accumulation of activated DC is one mechanism by which these cells
prevent immune pathology.
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