Following activation, T cells leave the lymph node and start trafficking via the bloodstream to the dermal vessels (Fig. 5.1b). Stimulation by keratinocyte-derived cytokines (IL-8, CCL27) leads to increased expression of adhesion molecules, including E-selectin and ICAM-1, in the post-capillary venules of inflamed skin. E-selectin is the target for cutaneous lymphocyte antigen (CLA) on the T-cell surface. Binding of CLA to E-selectin, as well as the interaction of the lymphocyte chemo-kine receptor (CCR10) with its ligand CCL27, slows circulating lymphocytes and causes their "rolling" along the endothelial wall.
As a result of increased exposure to chemokines, the affinity of LFA-1 for ICAM-1 is increased, probably mediated by a conformational change in the LFA-1 molecule. Bound T cells flatten and pass through the epithelium into the surrounding tissue - a process known as diapedesis. Once they have left the venule, T cells respond to chemokines; drawing them towards the site of inflammation in the dermis, and from there into the epidermis.
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