Get access

T regulatory cells and related immunoregulatory factors in polymorphic light eruption following ultraviolet A1 challenge

Authors


  • Funding sources None.
  • Conflicts of interest None declared.

Summary

Background

Polymorphic light eruption (PLE) is considered to be an autoimmune-mediated skin condition in which the normal ultraviolet (UV)-induced local immunosuppression appears to be absent, leading to recognition of photoinduced autoantigens and subsequent inflammation.

Objectives

To investigate T regulatory cells (Tregs) and related immunoregulatory factors in PLE lesions and controls.

Methods

Skin biopsies were performed in 13 patients with UVA1-challenged PLE, 12 female patients with chronic discoid lupus erythematosus (CDLE) and 11 healthy controls who had exposure to UVA1. Immunohistochemistry and four-colour immunofluorescence studies were performed.

Results

Patients with CDLE and UVA1-exposed controls showed significantly decreased epidermal immunoreactivity for CD1a compared with patients with PLE (= 0·0001). Four-colour immunofluorescence revealed a median percentage of CD4+CD25+FOXP3+ Tregs of 7·6% (range 3·7–13·6%) in PLE, a median of 11·7% (range 9·5–13·9%) in CDLE and a median of 3·4% (range 0–6·8%) in controls. Compared with UVA1-exposed controls, PLE and CDLE lesions showed significantly decreased transforming growth factor (TGF)-β1 immunoreactivity in the epidermis (= 0·0003). In PLE lesions, we observed significantly decreased interleukin (IL)-10 expression compared with CDLE (= 0·022). In the dermis, receptor activator of nuclear factor-κB ligand (RANKL) expression was increased in UVA1-exposed controls compared with PLE and CDLE (= 0·018).

Conclusions

Similar to CDLE lesions, UVA1-challenged PLE lesions display an altered immunoregulatory network, as indicated by decreased epidermal or dermal expression of TGF-β1, IL-10 and RANKL, and a relatively low number of Tregs, particularly when compared with other inflammatory skin conditions reported in the literature.

Get access to the full text of this article

Ancillary