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Review
. 2024 Oct 30;25(21):11670.
doi: 10.3390/ijms252111670.

Psoriasis and Seasonality: Exploring the Genetic and Epigenetic Interactions

Affiliations
Review

Psoriasis and Seasonality: Exploring the Genetic and Epigenetic Interactions

Michał Niedźwiedź et al. Int J Mol Sci. .

Abstract

Psoriasis is a multifactorial, chronic, and inflammatory disease that severely impacts patients' quality of life. The disease is caused by genetic irregularities affected by epigenetic and environmental factors. Some of these factors may include seasonal changes, such as solar radiation, air pollution, and humidity, and changes in circadian rhythm, especially in the temporal and polar zones. Thus, some psoriasis patients report seasonal variability of symptoms. Through a comprehensive review, we aim to delve deeper into the intricate interplay between seasonality, environmental factors, and the genetic and epigenetic landscape of psoriasis. By elucidating these complex relationships, we strive to provide insights that may inform targeted interventions and personalized management strategies for individuals living with psoriasis.

Keywords: air pollution; circadian rhythm; environmental factors; epigenetics; genetics; geoepidemiology; humidity; psoriasis; seasonality; solar radiation.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 2
Figure 2
Relation between environmental factors, genetic background, epigenetic modifications, and inflammatory reactions leading to deterioration of psoriatic skin symptoms. Environmental factors presenting seasonal patterns, such as solar radiation, humidity, air pollution, and circadian rhythm disturbances, influence genetic background and inflammatory drive within the skin [77,128,133,139,157,160,167]. Genes associated with psoriasis may be altered by environmental factors through epigenetic modifications [54,56,58,162,196]. Inflammation also causes a shift in gene expression, which leads to a positive feedback loop [66]. Inflammatory reactions cause hyperkeratinization and skin symptoms [66]. This figure was created with BioRender.com.
Figure 3
Figure 3
Factors leading to seasonal patterns of clinical deteriorations and improvements in patients with psoriasis. Due to the changes in environmental factors, such as humidity, solar exposure, and air pollution, patients may experience a reduction or deterioration of clinical symptoms. This figure was created with BioRender.com.
Figure 1
Figure 1
Influence of UV-R on the skin. When UV electromagnetic waves reach the skin, a small part of them are reflected, while the majority penetrate the skin and are absorbed by different molecules [77]. UV-B penetrates the skin to a depth of about 0.1 mm and UV-A to a depth of about 0.8 mm [79]. While UV-B is absorbed by most of the molecules within the skin, UV-A is not absorbed by DNA and most proteins but can be absorbed by endogenous porphyrins, oxidized fatty acids, and B vitamins [77,80]. The energy of absorbed UV is converted into heat, fluorescence, and chemical changes in the absorbing molecules, causing the formation of reactive oxygen species (ROS) such as superoxide anions, singlet oxygen, and hydroxyl radicals [77,80]. ROS can damage DNA and promote T-cell apoptosis [77,81,82,83,84]. Damaged keratinocytes produce and release several immunomodulators, such as tumor necrosis factors (TNF), 6-formylindolo[3,2-b]carbazole (FICZ), receptor activator of NF-κB ligand (RANKL), platelet-activating factors (PAFs), cis-urocanic acid (cis-UCA), and IL-10 [85,86,87]. TNFs, FICZ, and RANKL cause activation and migration of Langerhans cells to local lymph nodes [85,86,88,89]. PAFs and cis-UCA induce further release of TNFs, IL-10 and IL-4, which supports recruiting of cells such as Natural Killers (NKT) cells and regulatory B (Breg) and T (Treg) cells, which promote humoral and cell-mediated immunosuppression [85,90,91,92,93,94]. This figure was created with BioRender.com.

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