Blood 2002 Sep 26
Christopherson KW, Hood AF, Travers JB, Ramsey H, Hromas RA.
The signals which mediate T-cell infiltration during T-cell auto-immune diseases are poorly understood.
The chemokine CCL21 (originally isolated by us and others as Exodus-2/6Ckine/SLC/TCA4) is highly potent and highly specific for attracting T-cell migration.
However, it is thought to be expressed only in secondary lymphoid organs, directing naive T-cells to areas of antigen presentation.
It is not thought to play a role in T-cell effector function during a normal immune response.
In this study we tested the expression of T-cell chemokines and their receptors during T-cell auto-immune infiltrative skin diseases.
Using immunohistology it was found that the expression of CCL21 but not CCL19 or 20 was highly induced in endothelial cells of T-cell auto-immune diseases.
The receptor for CCL21, CCR7, was also found to be highly expressed on the infiltrating T-cells, the majority of which expressed the memory CD45Ro phenotype.
These data imply that the usual loss of CCL21 responsiveness in the normal development of memory T-cell effector function does not hold for auto-immune skin diseases.