Pathogenesis of solar urticaria: Classic perspectives and emerging concepts

Abstract

Solar urticaria is a rare, immunologically mediated photodermatosis in which activation of cutaneous mast cells is triggered by specific wavelengths of solar electromagnetic radiation. This manifests clinically as the rapid development of cutaneous itch, erythema and wheal formation after several minutes of sun exposure. Disease mechanisms in solar urticaria remain incompletely elucidated and there have been few recent investigations of its pathobiology. Historic passive transfer experiments performed during the twentieth century provide support for a ‘photoallergy’ model of disease pathogenesis, wherein molecular alteration of a putative chromophore by solar electromagnetic radiation produces mast cell activation via an IgE‐dependent mechanism. However, this model does not account for several observations made during passive transfer experiments nor does it explain a range of subsequent clinical and photobiological observations made in solar urticaria patients. Furthermore, increased understanding of the molecular dynamics underpinning cutaneous mast cell responses highlights the need to reformulate our understanding of solar urticaria pathogenesis in the context of this contemporary scientific landscape. In this review, we discuss the current understanding of solar urticaria pathogenesis and, by incorporating recent scientific and clinical observations, develop new hypotheses to drive future investigation into this intriguing disorder.

Urticaria

“…IgE autoantibodies might be produced to a skin-derived protein released upon stimulation, for example by cold 100 . In solar urticaria, molecular alteration of chromophores by solar electromagnetic radiation and their binding to surface-bound IgE on mast cells, leading to their activation, have been suggested 101 . In CholU, blockade of the sweat gland duct might lead to sweat reflux and leakage into the dermis inducing the symptoms of CholU due to production of a sweat antigen.…”

Solar Urticaria: An Ambispective Study in a Long-term Follow-up Cohort with Emphasis on Therapeutic Predictors and Outcomes

“…To our knowledge, this investigation is the most extensive evaluation of FcεRI in patients with SU to date. Previous publications have highlighted that SU symptoms are triggered with the participation of an IgE pathway (1)(2)(3)7). The association of clinical improvement with lowering FcεRI in omalizumab responders may reinforce the importance in pathophysiology of an IgE type 1 hypersensitivity in SU in real-life clinical practice.…”

“…Solar urticaria (SU) is a rare chronic inducible urticaria (CIndU) which is triggered by different wavelengths of light. The pathogenetic mechanisms implicated in SU are unknown, but the possibility that specific immunoglobulin E (IgE) antibodies triggered by photoallergens could bind mast cells leading to hive formation, in analogy to a type I immediate allergy, has been hypothesized ( 1 , 2 ). However, the precise cromophores that interact with light to form photoallergens, remain unknown.…”

Extracorporeal Photopheresis in Dermatological Diseases

“…Solar urticaria is a very rare chronic allergic reaction to sun exposure that causes pruritis, wheals, and erythema in sun-exposed areas. The cause of solar urticaria is not clearly defined, but the pathogenesis is stated as a type 1 IgE-mediated hypersensitivity reaction that involves Th2 cells interacting with B-cells, causing an inflammatory response and mast-cell activation [ 130 ]. First-line therapy includes antihistamines and corticosteroids.…”