Delayed‐type hypersensitivity reaction to St. John's wort extract confirmed by patch testing

O’Hagan, Thomas; Bisconti, Ilaria; Leck, Claire; Billahalli, Thippeswamy; Barnett, Sheena; Rajakulasingam, K.; Watts, Troy

doi:10.1111/cod.14172

Cited by 2 publications

(1 citation statement)

References 7 publications

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“…Skin barrier damage causes external antigens to easily pass through the damaged tight junction structure. These external antigens will be captured by Langerhans cells and presented to lymphocytes, which will then cause abnormal immune responses 26 . Thus, skin barrier injury may play a very important role in the occurrence of UV sensitivity and immune imbalance of CAD patients.…”

Section: Discussionmentioning

confidence: 99%

LncRNA‐WAKMAR2 regulates expression of CLDN1 to affect skin barrier through recruiting c‐Fos

Wang

et al. 2022

Contact Dermatitis

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Background: Chronic actinic dermatitis (CAD) is an immune-mediated photo-allergic skin disease. In the clinic, the treatment of this disease is hampered by the lack of proper understanding of the skin barrier dysfunction mechanism.Objective: To illuminate the mechanism of skin barrier dysfunction in CAD.Methods: Transcriptome sequencing and protein profiling were used to detect skin barrier injury-related genes. RNA pull down, a promoter-reporter gene assay, and chromatin isolation by RNA purification-sequencing were used to elucidate the effect of WAKMAR2 in skin barrier functionality.Results: Transcriptome sequencing from patient's tissues showed a significantly decreased expression of WAKMAR2. Down-regulation of WAKMAR2 destroyed the keratinocyte barrier. Moreover, WAKMAR2 can directly bind to the c-Fos protein.This novel long non-coding RNA (LncRNA)-protein complexes were targeted to the CLDN1 promotor. Overexpression of WAKMAR2 enhanced the promoter activity of CLDN1, while the addition of AP-1 inhibitor could reverse this phenomenon. Furthermore, our in vivo results suggested that expression of WAKMAR2 was required for the repair of skin damage in mice induced by ultraviolet irradiation. Conclusions:We identified a crucial LncRNA (WAKMAR2) for the protection of the skin barrier in vitro and in vivo. Mechanically, it can specifically interact with c-Fos protein for the regulation of CLDN1, a finding which could be applied for CAD treatment.

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Section: Discussionmentioning

confidence: 99%

LncRNA‐WAKMAR2 regulates expression of CLDN1 to affect skin barrier through recruiting c‐Fos

Wang

et al. 2022

Contact Dermatitis

View full text Add to dashboard Cite

show abstract

Side effects of vitamins, amino acids, nutrition, and complementary and alternative medicine

Waller

2023

Side Effects of Drugs Annual

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Delayed‐type hypersensitivity reaction to St. John's wort extract confirmed by patch testing

Cited by 2 publications

References 7 publications

LncRNA‐WAKMAR2 regulates expression of CLDN1 to affect skin barrier through recruiting c‐Fos

LncRNA‐WAKMAR2 regulates expression of CLDN1 to affect skin barrier through recruiting c‐Fos

Side effects of vitamins, amino acids, nutrition, and complementary and alternative medicine

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