All About Multiple Sclerosis

More MS news articles for November 2002

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

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12393410&dopt=Abstract

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.