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Protein Design Laboratories, Inc., Fremont, CA 94555
The demonstrated role of E- and P-selectin ligands in the
recruitment of Th1 cells raises the question of tissue specificity
determination by pathogenic T cells. We took advantage of the fact that
chronic Th1-mediated inflammation in the scid/scid
CD4+CD45RBhigh T cell transfer model can occur
at multiple tissue sites, resembling inflammatory bowel disease in the
colon and psoriasis in the skin. We show that the majority of
infiltrating effector T cells from psoriatic skin expresses high levels
of functional P-selectin ligand (87 ± 3%), detected by
P-selectin-Ig (PIg), while a significantly smaller subset of T cells
from colitic lesions expresses this ligand (24 ± 2%). Similarly,
E-selectin ligand is preferentially expressed on CD4+ T
cells infiltrating the skin (24 ± 2%), but only on very few
CD4+ T cells infiltrating the colon (CIT; 1.3 ±
0.8%). In contrast, CD4+ T cells infiltrating the skin
express 
4ß7 at a significantly lower level
than CIT (mean fluorescence intensity, 28 vs 61, respectively),
although, interestingly, Eß7 was expressed
at high levels on both populations. Analysis of the disease-inducing
potential of PIg+ and PIg- CD4+
CIT cells revealed that both populations not only express similar
levels of the gut-homing molecule 4ß7
(mean fluorescence intensity, 50 vs 56, respectively), but do not
differ in their capacity to express IFN-
. Furthermore, CIT depleted
of cells expressing functional P-selectin ligand were able to induce
colitis upon transfer, suggesting that induction of colitis in this
model may be independent of E- and P-selectin. These results indicate
that adhesion molecule expression and the homing pattern of
inflammatory T cells are regulated by the local environment
independently of their inflammatory capacity.
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