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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Endothelial induction of the T-cell chemokine CCL21 in T-cell autoimmune diseases.

The signals that mediate T-cell infiltration during T-cell autoimmune 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 stimulating 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 autoimmune infiltrative skin diseases. By using immunohistology it was found that the expression of CCL21 but not CCL19 or 20 was highly induced in endothelial cells of T-cell autoimmune diseases. The receptor for CCL21, CCR7, was also found to be highly expressed on the infiltrating T cells, most 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 autoimmune skin diseases.[1]


  1. Endothelial induction of the T-cell chemokine CCL21 in T-cell autoimmune diseases. Christopherson, K.W., Hood, A.F., Travers, J.B., Ramsey, H., Hromas, R.A. Blood (2003) [Pubmed]
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