Early time course of recruitment of immune surveillance in human skin after chemical provocation.

As part of the defence function of skin it seems probable that mechanisms exist for the rapid recruitment of immune surveillance to 'inspect' any foreign substance that penetrates the skin. In the present study, evidence of such mechanisms was sought by following the time course of early changes in distribution of immune cells, expression of cell adhesion molecules and cytokines after epicutaneous challenge with provoking chemicals to which subjects were known to be either specifically 'sensitive' or 'non-sensitive'; anthralin, an irritant chemical, was used as control. Fifty-seven individuals were studied and there were at least five biopsy samples at each time point. Regardless of whether individuals were sensitive or not, or of the type of chemical, dermal microvascular endothelial cells showed increased expression of the adhesion molecules ELAM-1 and VCAM-1 within 2 h, and ICAM-1 within 8 h. The intensity of immunohistochemical staining increased progressively up to 24 h. More vessels stained for ICAM-1 than for VCAM-1 or ELAM-1, implying that not every vessel expressed all three cell adhesion molecules. Another early change, observed 2 h after irritant challenge, was a significant increase in numbers of CD1a+ dendritic cells in the superficial dermis from a median of 3/high power field (hpf) to 9.5/hpf (P < 0.03). This was not observed with 'weak' provoking substances, such as nickel, but did occur with the potent provoking agent dinitrochlorobenzene (DNCB). Thus, as little as 2 h after contact with provoking chemicals, the skin activates cellular mechanisms to increase T cell infiltration for the presumed purpose of immune surveillance. These mechanisms are not dependent upon specific immune sensitivity and reflect a capacity of skin cells to respond to chemical provocation.