How does traditional phototherapy work?

Immunomodulation locally, and possibly systemically, is the primary mechanism of action of phototherapy. Effects on keratinocyte proliferation and differentiation are likely secondary to the immunomodulatory effects. Immunomodulatory effects include: T-cell apoptosis (CD8+ in epidermis, CD4+ in dermis, CD25+ in both epidermis and dermis), inhibition and depletion of antigen-presenting cells (Langerhans cells in epidermis, dermal dendritic cells in dermis), release of immunosuppressive cytokines (interleukin [IL]-10 and IL-4, reduced expression of tumor necrosis factor–α [TNF-α]), interferon (IFN)-γ, and IL-12 locally, photoisomerization of trans-urocanic acid to cis-uracanic acid (which suppresses cellular immune responses, such as antigen presentation by Langerhans cells), and upregulation of CD95L (Fas ligand that binds to the Fas receptor on T cells inducing apoptosis).


Ozawa M, Ferenczi K, Kikuchi T, et al: 312-nanometer ultraviolet B light (narrow-band UVB) induces apoptosis of T cells within psoriatic lesions, J Exp Med 89:711–718, 1999.

Walters IB, Ozawa M, Cardinale I, et al: Narrowband (312-nm) UV-B suppresses interferon gamma and interleukin (IL) 12 and increases IL-4 transcripts: differential regulation of cytokines at the single-cell level: Arch Dermatol 139:155–161, 2003.