Ultraviolet-Radiation-Induced Erythema and Suppression of Contact Hypersensitivity Responses in Patients with Polymorphic Light Eruption

Abstract

Ultraviolet-radiation suppresses cell-mediated immunity in healthy humans. It has been postulated that, in the short term, this immunosuppression prevents autoimmune responses to ultraviolet-radiation damaged skin. Patients with polymorphic light eruption (PLE) demonstrate abnormal responses to ultraviolet-radiation suggestive of an immune response to an ultraviolet-radiation-induced antigen. We investigated whether PLE patients (n=22) were resistant to ultraviolet-radiation-induced immunosuppression compared to skin-type, aged-matched controls (n=23). Groups of patients and controls (six subjects per group) received a single dose of solar-simulated ultraviolet-radiation of either 0, 0.6, 1 or 2 minimal erythema doses (MED). Erythema was quantified using a reflectance meter and all volunteers were sensitised on the irradiated site with dinitrochlorobenzene. Contact hypersensitivity responses (CHS) to dinitrochlorobenzene were quantified after challenge using ultrasound. Ultraviolet-radiation-induced erythema was comparable in patients and controls. CHS was comparable in unirradiated patients and controls. UVR-induced a dose-dependent suppression of CHS in all volunteers but patients were more resistant to immunosuppression after 1MED. Exposure to 1MED suppressed CHS by 78% in controls but induced less suppression in patients (44%, p < 0.01). Our data suggest that PLE patients have a flaw in their immunoregulatory response to ultraviolet-radiation it is only apparent over a narrow dose range around 1 MED.

An Optimal Method for Experimental Provocation of Polymorphic Light Eruption

“…The pathogenesis of PLE is unclear, but histologic and immunologic studies suggest that the normal UVRinduced suppression of cell-mediated immunity is impaired and, as a result, these patients develop a T-cell mediated response to a UVR-activated antigen (photoantigen). 4,5 Investigations into the pathogenesis of PLE have been frustrated by the lack of reliable laboratory methods for the induction of clinical lesions. The results of such studies have varied considerably.…”

Photohardening of polymorphic light eruption patients decreases baseline epidermalLangerhans cell density while increasing mast cell numbers in the papillary dermis

“…The pathogenesis underlying polymorphic light eruption (PLE) is thought to involve an inability of ultraviolet (UV) radiation to suppress the immune response against UV-induced photoantigens (1)(2)(3)(4). A key cellular event in UV immunosuppression is the migration of Langerhans cells (LC) from the epidermis to the skin-draining lymph nodes (5) where they mediate the activation of immunoregulatory T cells (6).…”

Explaining a possible protective role of polymorphous light eruption against skin cancer

“…The original idea that cytokines instrumental for these migratory responses and ensuing tolerance would be weaker in PLE was not confirmed, instead the PLE skin showed an IL-1/IL1-receptor a ratio which indicated a basic bias toward inflammatory reactions [14], which indicates an unbalance in the skin reaction, more aberrant in the proinflammatory arm than in the suppressive arm. Two British groups provided the important functional evidence that PLE patients indeed show a diminished UV-induced suppression of sensitization to a contact allergen with physiological UV dosages around the threshold dose for an erythema [15,16], very much in contrast to the earlier mentioned group of people who had skin carcinomas removed.…”