Methods:LC-like dendritic cells (LDCs) were generated from mouse bone marrow cells. Mice were primed with ovalbumin (OVA) peptide-pulsed LDCs, which had been treated with tacrolimus or betamethasone, via the hind footpad. After 5 days, the cytokine response in the draining popliteal lymph nodes was investigated by enzyme-linked immunosorbent assay. The expression of LDC surface molecules was investigated using reverse transcriptase polymerase chain reaction.
Results: Administration of OVA peptide-pulsed LDCs, which had been treated with betamethasone, into the hind footpads of mice inhibited Th2 development as represented by down-regulation of interleukin (IL)-4 production as well as Th1 development as represented by down-regulation of interferon (IFN)-γ production. However, unlike the LDCs treated with betamethasone, those treated with tacrolimus did not inhibit Th1/Th2 cell development. The inhibition of Th1 cell and Th2 cell development by betamethasone was associated with suppression of CD40 and TIM-4 expression, respectively, in LDCs.
Conclusion: These results suggest that topical application of betamethasone to lesional skin would be beneficial for control of atopic dermatitis by acting on epidermal LCs and inhibiting the development of Th2 cells.