Background: It has been proposed that the innate immune system plays a central role in driving the autoimmune T-cell cascade leading to psoriasis; however, there is no direct evidence for this. Observations:We observed aggravation and spreading of a psoriatic plaque when treated topically with the toll-like receptor (TLR) 7 agonist imiquimod. The exacerbation of psoriasis was accompanied by a massive induction of lesional type I interferon activity, detected by MxA expression after imiquimod therapy. Since imiquimod induces large amounts of type I interferon production from TLR7-expressing plasmacytoid dendritic cell precursors (PDCs), the natural interferon-producing cells of the peripheral blood, we asked whether PDCs are pres-ent in psoriatic skin. We identified high numbers of PDCs in psoriatic skin lesions (up to 16% of the total dermal infiltrate) based on their coexpression of BDCA2 and CD123. By contrast, PDCs were present at very low levels in atopic dermatitis and not detected in normal human skin. Conclusions:This study shows that psoriasis can be driven by the innate immune system through TLR ligation. Furthermore, our finding that large numbers of PDCs infiltrate psoriatic skin suggests a role of lesional PDCs as type I interferon-producing targets for the TLR7 agonist imiquimod.

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In the 1950s, based on the theory of stimulating radiant energy published by Albert Einstein in 1916, the collaboration of physicists and electrical engineers, searching for monochromatic radiation to study the spectra of molecules, led to the invention of the first laser in 1960. Ophthalmologists and dermatologists were the first to study the biological effects and therapeutic possibilities of laser beams. The construction of new laser systems emitting energy at different wavelengths or with different durations, as well as the development of new concepts of the biomedical effects, led to its broad use in surgery in the treatment of vascular and pigmented lesions as well as cosmetic applications.

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