Ultraviolet light protection by a sunscreen prevents interferon‐driven skin inflammation in cutaneous lupus erythematosus

Abstract

provided by future studies. For example, abnormal cytoplasmic Ca 2+ may be examined by mutagenesis and functional studies.Abnormal cytoplasmic Ca 2+ caused by haploinsufficiency of SPCA1 may alter post-translational modifications, including glycosylation, folding, trafficking and sorting, in cell adhesion molecules, leading to acantholytic changes seen in HHD (11-13). This study showed that different mutations in HHD result in distinct expression of mRNA and protein, which may relate to clinical phenotypes. AcknowledgementSee supporting information for details (Data S2). Author contributionMM, SN and KT performed the researches. HO and SI contributed samples. T. Hamada, CH and MF designed this study. MM and T. Hashimoto wrote the paper. Conflict of interestThe authors state no conflict of interest. Abstract: Irradiation with ultraviolet (UV) light is an important exacerbating factor in cutaneous lupus erythematosus (CLE) and induces various effects in the skin of patients with the disease, such as cell death and inflammation. Recently, we demonstrated the ability of a broad-spectrum sunscreen to prevent UV-induced damage both in patients with CLE and healthy controls (HCs). The aim of this study was to evaluate whether the UV-dependent activation of interferon (IFN)-driven inflammation in CLE can also be prevented by application of the sunscreen. In 20 patients with different subtypes of CLE and 10 HCs, defined areas on the upper back were treated with a broad-spectrum liposomal sunscreen 20 min prior to a combined standardized UVA/UVB irradiation. Immunohistological analyses using antibodies directed against MxA, CD11c, CD123 and CD68 were performed from skin biopsies taken from areas before UV irradiation as well as from sunscreen-treated and sunscreen-untreated areas 24 and 72 h after UV irradiation. The expression of MxA was completely prevented by the sunscreen applied prior to UV irradiation in CLE patients and HCs. Additionally, sunscreen protection significantly diminished the number of the CD11c-and CD123-positive dendritic cells, which are suggested to be a major source of type I/III IFNs, in UV-irradiated skin of patients with CLE. Moreover, the application of the sunscreen prevented the increase in CD68-positive macrophages in both groups 72 h after UV irradiation. The data of this study demonstrate that UV protection reduces lesional tissue damage and inhibits the typical IFN-driven inflammatory response in CLE.

Pathogenesis and targeted treatment of skin injury in SLE

“…The majority of patients with SLE show skin hypersensitivity to sunlight, 6,18 and ultraviolet light (UV) is well known to be the most important environmental factor involved in triggering skin injury or even inducing systemic inflammation in these patients. 19 Large cohort studies and randomized controlled trials in patients with SLE have demonstrated that standardized UV-A and UV-B photoprovocation represents a useful method of evaluating photosensitivity, 19 and could be useful in the future for diagnostic testing and in clinical trials.…”

S2k guideline for treatment of cutaneous lupus erythematosus – guided by the European Dermatology Forum (EDF) in cooperation with the European Academy of Dermatology and Venereology (EADV)

“…A randomized controlled trial demonstrated that the application of a broad‐spectrum sunscreen with a high protection factor prevents UV‐induced skin lesions under standardized conditions . The clinical results have recently been confirmed by an open‐label study with a liposomal sunscreen, supported by histology and immunohistochemistry …”

Review of treatment for discoid lupus erythematosus

“…A more recent study demonstrated decreased interferon-mediated inflammation in biopsies of sunscreen-protected skin (6). While both UVA and UVB blocking, there is no further literature available regarding this compound in DLE.…”