Annals of dermatology · 2026
The Role of Inflammasome in the Pathogenesis of Alopecia Areata: NLRP3 and Its Cascade Contribute to the Onset and Early Stage of Alopecia Areata.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Lim Ji-Hoon, Kang Da-Hyun, Moon Haena, Kwon Soon-Hyo, Lew Bark-Lynn
Аннотация
BACKGROUND: The inflammasome, a multiprotein complex, is crucial in the pathogenesis of various autoinflammatory disorders. In particular, the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome has recently been associated with diseases such as psoriasis, vitiligo, lupus, and alopecia areata (AA).
OBJECTIVE: The objective of this study is to investigate the potential involvement of the inflammasome in the pathogenesis of AA and to determine its correlation with clinical manifestations.
METHODS: A total of 144 patients with AA and 22 healthy controls were included. Scalp skin and serum samples were collected to assess the levels of NLRP3-related molecules in lesional tissue and blood, respectively. Additionally, we performed immunostaining to measure the expression of NLRP3 and caspase-1 in the outer root sheath (ORS).
RESULTS: Lesional interleukin-1β expression was significantly elevated in patients with AA at all stages compared with controls. In the progressive stage, lesional C-X-C motif chemokine ligand 10 levels were markedly higher than those in controls and other stages. Serum interferon-γ levels were also significantly increased during the progressive stage of AA compared with controls. Immunostaining revealed strong NLRP3 and caspase-1 positivity in the ORS during the initial and progressive stages of AA, in contrast to the recovery stage.
CONCLUSION: These results highlight the functional role of the inflammasomes in the pathogenesis of AA.
OBJECTIVE: The objective of this study is to investigate the potential involvement of the inflammasome in the pathogenesis of AA and to determine its correlation with clinical manifestations.
METHODS: A total of 144 patients with AA and 22 healthy controls were included. Scalp skin and serum samples were collected to assess the levels of NLRP3-related molecules in lesional tissue and blood, respectively. Additionally, we performed immunostaining to measure the expression of NLRP3 and caspase-1 in the outer root sheath (ORS).
RESULTS: Lesional interleukin-1β expression was significantly elevated in patients with AA at all stages compared with controls. In the progressive stage, lesional C-X-C motif chemokine ligand 10 levels were markedly higher than those in controls and other stages. Serum interferon-γ levels were also significantly increased during the progressive stage of AA compared with controls. Immunostaining revealed strong NLRP3 and caspase-1 positivity in the ORS during the initial and progressive stages of AA, in contrast to the recovery stage.
CONCLUSION: These results highlight the functional role of the inflammasomes in the pathogenesis of AA.