The Effect of Solar-Simulated Radiation on the Elicitation Phase of Contact Hypersensitivity does not Differ Between Controls and Patients with Polymorphic Light Eruption

Abstract

It has been suggested that polymorphic light eruption (PLE) is characterized by a failure of ultraviolet radiation (UVR)-induced immunosuppression, resulting in a type-IV hypersensitivity response to photoinduced antigens. We measured the effect of solar-simulated radiation (SSR) on the elicitation phase of contact hypersensitivity to 2,4-dinitrochlorobenzene (DNCB), in ten PLE patients and 11 controls. Subjects were given a sensitizing dose of DNCB, and 3 wk later were exposed to 0.75 and 2 minimum erythema doses (MED) of SSR on the upper inner arm. Immediately and 24 h later these sites, and a non-irradiated control site, were challenged with DNCB. The resulting increase in skin thickness was measured with high-frequency ultrasound. Overall, 2 MED caused 17%-20% suppression of elicitation responses (compared with 93% suppression of sensitization reported previously), but the effect of SSR varied greatly between subjects, with some subjects showing potentiated responses, which may be of relevance to false-positive reactions in photopatch testing. In a repeated measures general linear model, SSR overall caused significant suppression of responses (p<0.001); there was less suppression in older subjects (p=0.009) but there was no significant difference between PLE patients and age-matched normal controls. These results contrast with our previous finding of a resistance to UVR-induced suppression of sensitization to DNCB in PLE. This difference may reflect the greater importance of Langerhans cells in the sensitization phase, and is consistent with the hypothesis that PLE arises from impaired suppression of Langerhans cell activation or migration.

Photodermatoses and Skin Cancer

“…These results contrasted with previous findings of the same group that had indicated a resistance to UV-induced suppression of sensitization to DNCB in PLE. This difference may reflect the greater importance of Langerhans cells in the sensitization phase, and is consistent with the hypothesis that PLE arises from impaired suppression of Langerhans cell activation or migration (Palmer, 2005). The reason for the occurrence of PLE appears likely to be genetic with a significant environmental component, with 70% of the population perhaps having a tendency to the condition but not all expressing it because of poor penetrance.…”

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

“…20 As shown in previous studies, we observed that epidermal Langerhans cells are also significantly diminished in CDLE. [3][4][5]22 In skin lesions of patients with PLE, we have investigated Tregs and immunoregulatory factors such as TGF-b1, IL-10 and RANKL. 21 We observed significantly reduced levels of CD68+ cells in the epidermis of PLE lesions compared with CDLE and controls.…”

“…[3][4][5][6] T regulatory cells (Tregs) are considered to be of vital importance for maintaining immunological self-tolerance and preventing autoimmune diseases. The disease occurs at all degrees of latitude, particularly affects the young female population and can significantly influence quality of life.…”

Immunologically Mediated Photodermatoses

“…However, photosensitive diseases occur when the human skin reacts abnormally to optical radiation: in particular, UV radiation or visible light. [1][2][3][4][5][6][7] Photodermatoses may be subdivided into four groups. [1] The first group consists of immunologically mediated photodermatoses (IMP), also previously known as idiopathic or primary photodermatoses.…”