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UVA1 phototherapy

Jean Krutmann, MD
Akimichi Morita, MD, PhD
Section Editor
Craig A Elmets, MD
Deputy Editor
Rosamaria Corona, MD, DSc


Ultraviolet A1 (UVA1) is a newer form of phototherapy that uses only the longer, non-erythemogenic UV wavelengths (340 to 400 nm), thus reducing the risk of sunburn reactions associated with the shorter-wavelength UVA2 (320 to 340 nm) and UVB (290 to 320 nm). It is important to note that the UVA1 light sources are not equivalent to the light sources used for cosmetic purposes in tanning parlors and home units, which emit UVA2 wavelengths and often some UVB as well in addition to UVA1. The therapeutic effect of UVA1 is due to its ability to penetrate into the dermis deeper than UVB and target cells that reside in or infiltrate the dermis, including dendritic cells, fibroblasts, mast cells, and T and B lymphocytes [1].

This topic reviews the mechanism of action, clinical indications, and adverse effects of UVA1 phototherapy. PUVA therapy and broadband and narrowband UVB phototherapy are discussed separately. (See "Psoralen plus ultraviolet A (PUVA) photochemotherapy" and "UVB therapy (broadband and narrowband)".)


The long-wavelength ultraviolet A1 (UVA1) radiation (340 to 400 nm) is able to penetrate into the dermis deeper than short-wavelength UVA2 (320 to 340 nm) and UVB (290 to 320 nm). UVA1 exerts its biologic effects on a variety of cells, including T and B lymphocytes, fibroblasts, dendritic cells, and immature mast cells [2-4].

UVA1-induced apoptosis — The ability of UVA1 to induce apoptosis of infiltrating T cells is thought to underlie its therapeutic efficacy for the treatment of T-cell mediated inflammatory and neoplastic skin diseases, such as atopic dermatitis and mycosis fungoides. Malignant CD4+ T cells appear to be more sensitive to UVA1 radiation-induced apoptosis than normal CD4+ T cells [5].

In vitro, UVA1 has been shown to induce immediate and delayed cell apoptosis through at least two different mechanisms. In the first, UVA1 induces the generation of singlet oxygen species, which depolarize mitochondrial membranes and trigger immediate cell apoptosis through the activation of the FAS/FAS ligand system [2]. This mechanism is termed preprogrammed cell death and appears to be specific of UVA1 phototherapy, since it is not observed with UVB or PUVA phototherapy. The second mechanism involves the production of superoxide anions, which damage the mitochondrial membrane resulting in the release of cytochrome C and activation of a caspase-dependent apoptotic pathway [3].


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Literature review current through: Sep 2016. | This topic last updated: Oct 20, 2015.
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