In both murine and human experimental systems, acute, low dose exposure of skin to ultraviolet B light (UVB) impairs the induction of
allergic contact dermatitis (ACD) by
haptens such as
dinitrochlorobenzene (
DNCB) in a significant proportion of individuals. By light microscopy, epidermal Langerhans cells (LC) have been reported to be depleted by UVB exposure as well as by epicutaneous
hapten application, implying that LC may be the locus of action of the effects of both UVB and
DNCB. However, light microscopy can not readily distinguish cell density changes secondary to LC
necrosis from changes resulting from down-modulation of expression of LC surface molecules. Using a highly sensitive immunogold electron microscopic approach, we have evaluated the differential effects of UVB and/or
DNCB on human epidermal LC. The results reveal that
DNCB alone caused significant up-regulation of cell surface HLA class II expression on a very small number of LC, the major fraction of LC expressing normal levels of HLA class II. Furthermore,
DNCB alone caused a modest reduction in the density of LC at the treated sites without evidence of cell
necrosis. Treatment with UVB alone or UVB exposure followed by
DNCB resulted in a reduction in the density of LC, with widespread evidence of LC
necrosis. However, the few remaining intact LC were all intensely HLA class II-positive after UVB exposure followed by
DNCB, whereas treatment with UVB alone did not result in changes in LC HLA class II expression. The findings that after
DNCB painting only a small proportion of the LC were strongly HLA class II-positive, but after UVB exposure followed by
DNCB all intact LC displayed significant up-regulation of cell surface HLA class II expression, imply that UVB exposure inhibits the migration of epidermal LC. This is consistent with the view that
DNCB fails to induce ACD when
hapten is painted on UVB-exposed skin because insufficient LC are available to initiate T cell activation in the draining lymph node.